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1. Primary Aldosteronism Influences Cardiac Structure, Function, and Disease Risk: Evidence From Mendelian Randomization Analysis

Author: Rui Shen, Chengliang Pan, Jian Yu, Chen Dong, Zhiyang Li, Jiangmei Zhang, Qian Dong, Kunwu Yu, and Qiutang Zeng
Subjects: atrial fibrillation, cardiovascular disease, cardiovascular magnetic resonance, coronary artery disease, heart failure, mendelian randomization, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract: ABSTRACT Although observational studies have linked primary aldosteronism (PA) with cardiovascular diseases (CVDs), the causality remains uncertain. In this study, we aimed to investigate whether PA is causally associated with CVD risk and cardiac magnetic resonance (CMR) parameters using the Mendelian randomization (MR) method. Independent and genome‐wide significant single nucleotide polymorphisms for PA were extracted from genome‐wide association study (GWAS) summary statistics. Genetic associations with the CVDs and CMR parameters were obtained from recent large‐scale GWASs or genetic consortia. Inverse‐variance weighted (IVW) method was utilized for the preliminary estimates, and multiple sensitivity analyses (including weighted median, Cochran's Q test, MR‐Egger, MR‐PRESSO, and leave‐one‐out analysis) were conducted to verify the robustness of the results. The MR analyses using the IVW method showed that genetically predicated PA was significantly associated with atrial fibrillation (OR = 1.046, 95% CI: 1.029–1.062, padj
Published: 2024
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2. IL-4-Induced Gene 1: A Potential Player in Myocardial Infarction

Author: Rui Shen, Yan Ding, Qian Dong, Yue Wang, Jian Yu, Chengliang Pan, Yifan Cai, Zhiyang Li, Jiangmei Zhang, Kunwu Yu, and Qiutang Zeng
Subjects: myocardial infarction, il4i1, laao, macrophage, cd4+ t cell, ferroptosis, immunometabolism, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract: Myocardial infarction (MI), a severe outcome of cardiovascular disease, poses a serious threat to human health. Uncontrolled inflammation and excessive cardiomyocyte death, following an infarction event, significantly contribute to both the mortality rate and complications associated with MI. The protein IL-4-induced gene 1 (IL4I1 or FIG1) serves as a natural inhibitor of innate and adaptive immunity, playing a crucial role in CD4+ T cell differentiation, macrophage polarization, and ferroptosis inhibition. Previous studies have linked IL4I1 to acute MI. This review summarizes evidence from both basic and clinical research, highlighting IL4I1 as a critical immunoregulatory enzyme that not only regulates inflammatory responses, but also potentially mitigates MI-induced damage.
Published: 2024
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3. Type 2 Diabetes, Circulating Metabolites, and Calcific Aortic Valve Stenosis: A Mendelian Randomization Study

Author: Rui Shen, Chengliang Pan, Guiwen Yi, Zhiyang Li, Chen Dong, Jian Yu, Jiangmei Zhang, Qian Dong, Kunwu Yu, and Qiutang Zeng
Subjects: type 2 diabetes, calcific aortic valve stenosis, mediation, Mendelian randomization, metabolites, blood pressure, Microbiology, QR1-502
Abstract: Epidemiological studies have shown an association between type 2 diabetes (T2D) and calcific aortic valve stenosis (CAVS), but the potential causal relationship and underlying mechanisms remain unclear. Therefore, we conducted a two-sample and two-step Mendelian randomization (MR) analysis to evaluate the association of T2D with CAVS and the mediating effects of circulating metabolites and blood pressure using genome-wide association study (GWAS) summary statistics. The inverse variance weighted (IVW) method was used for the primary MR analysis, and comprehensive sensitivity analyses were performed to validate the robustness of the results. Our results showed that genetically predicted T2D was associated with increased CAVS risk (OR 1.153, 95% CI 1.096–1.214, p < 0.001), and this association persisted even after adjusting for adiposity traits in multivariable MR analysis. Furthermore, the two-step MR analysis identified 69 of 251 candidate mediators that partially mediated the effect of T2D on CAVS, including total branched-chain amino acids (proportion mediated: 23.29%), valine (17.78%), tyrosine (9.68%), systolic blood pressure (8.72%), the triglyceride group (6.07–11.99%), the fatty acid group (4.78–12.82%), and the cholesterol group (3.64–11.56%). This MR study elucidated the causal impact of T2D on CAVS risk independently of adiposity and identified potential mediators in this association pathways. Our findings shed light on the pathogenesis of CAVS and suggest additional targets for the prevention and intervention of CAVS attributed to T2D.
Published: 2024
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4. Case report: Malignant vasovagal reflex syndrome during percutaneous transcatheter closure of patent foramen ovale

Author: Zhiyang Li, Qian Dong, Lun Huang, Qiutang Zeng, and Kunwu Yu
Subjects: vasovagal reflex syndrome, percutaneous transcatheter closure of patent foramen ovale, cardiac arrest, ventricular tachycardia, malignant arrhythmia, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract: Malignant vasovagal reflex syndrome can be induced by pulling of cardiac tissue during percutaneous transcatheter closure of patent foramen ovale. In this case, a patient presented with a malignant vasovagal reflex syndrome characterized by decreased heart rate, cardiac arrest, and ventricular tachycardia. Therefore, it's particularly important to observe patients' heart rate and timely deal with vasovagal reflex syndrome during the operation.
Published: 2023
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5. Prevalence and prognosis of molecularly defined familial hypercholesterolemia in patients with acute coronary syndrome

Author: Cheng Wang, Puliang Yu, Lizhi Hu, Minglu Liang, Yi Mao, Qiutang Zeng, Xiang Wang, Kai Huang, Jin Yan, Li Xie, Fengxiao Zhang, and Feng Zhu
Subjects: acute coronary syndrome, cardiovascular events, familial hypercholesterolemia, low-density lipoprotein cholesterol, lipid, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract: BackgroundFamilial hypercholesterolemia (FH) can elevate serum low-density lipoprotein cholesterol (LDL-C) levels, which can promote the progression of acute coronary syndrome (ACS). However, the effect of FH on the prognosis of ACS remains unclear.MethodsIn this prospective cohort study, 223 patients with ACS having LDL-C ≥ 135.3 mg/dL (3.5 mmol/L) were enrolled and screened for FH using a multiple-gene FH panel. The diagnosis of FH was defined according to the ACMG/AMP criteria as carrying pathogenic or likely pathogenic variants. The clinical features of FH and the relationship of FH to the average 16.6-month risk of cardiovascular events (CVEs) were assessed.ResultsThe prevalence of molecularly defined FH in enrolled patients was 26.9%, and coronary artery lesions were more severe in patients with FH than in those without (Gensini score 66.0 vs. 28.0, respectively; P < 0.001). After lipid lowering, patients with FH still had significantly higher LDL-C levels at their last visit (73.5 ± 25.9 mg/dL vs. 84.7 ± 37.1 mg/dL; P = 0.013) compared with those without. FH increased the incidence of CVEs in patients with ACS [hazard ratio (HR): 3.058; 95% confidence interval (CI): 1.585–5.900; log-rank P < 0.001].ConclusionFH is associated with an increased risk of CVEs in ACS and is an independent risk factor for ACS. This study highlights the importance of genetic testing of FH-related gene mutations in patients with ACS.
Published: 2022
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6. Effects of IL-38 on Macrophages and Myocardial Ischemic Injury

Author: Zhiyang Li, Yan Ding, Yudong Peng, Jian Yu, Chengliang Pan, Yifan Cai, Qian Dong, Yucheng Zhong, Ruirui Zhu, Kunwu Yu, and Qiutang Zeng
Subjects: interleukin-38, macrophages, myocardial infarction, myocardial ischemia–reperfusion injury, ventricular remodeling, inflammation, Immunologic diseases. Allergy, RC581-607
Abstract: Macrophages play an important role in clearing necrotic myocardial tissues, myocardial ischemia–reperfusion injury, and ventricular remodeling after myocardial infarction. M1 macrophages not only participate in the inflammatory response in myocardial tissues after infarction, which causes heart damage, but also exert a protective effect on the heart during ischemia. In contrast, M2 macrophages exhibit anti-inflammatory and tissue repair properties by inducing the production of high levels of anti-inflammatory cytokines and fibro-progenitor cells. Interleukin (IL)-38, a new member of the IL-1 family, has been reported to modulate the IL-36 signaling pathway by playing a role similar to that of the IL-36 receptor antagonist, which also affects the production and secretion of macrophage-related inflammatory factors that play an anti-inflammatory role. IL-38 can relieve myocardial ischemia–reperfusion injury by promoting the differentiation of M1 macrophages into M2 macrophages, inhibit the activation of NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) inflammasome, and increase the secretion of anti-inflammatory cytokines, such as IL-10 and transforming growth factor-β. The intact recombinant IL-38 can also bind to interleukin 1 receptor accessory protein-like 1 (IL-1RAPL1) to activate the c-jun N-terminal kinase/activator protein 1 (JNK/AP1) pathway and increase the production of IL-6. In addition, IL-38 regulates dendritic cell-induced cardiac regulatory T cells, thereby regulating macrophage polarization and improving ventricular remodeling after myocardial infarction. Accordingly, we speculated that IL-38 and macrophage regulation may be therapeutic targets for ameliorating myocardial ischemic injury and ventricular remodeling after myocardial infarction. However, the specific mechanism of the IL-38 action warrants further investigation.
Published: 2022
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7. Interleukin-27 Ameliorates Atherosclerosis in ApoE-/- Mice through Regulatory T Cell Augmentation and Dendritic Cell Tolerance

Author: Wenbin Xu, Ruirui Zhu, Zhengfeng Zhu, Kunwu Yu, Yue Wang, Yan Ding, Jian Yu, Hongxia Tang, Qiutang Zeng, and Yucheng Zhong
Subjects: Pathology, RB1-214
Abstract: Atherosclerosis, which is characterized by chronic inflammation in the arterial wall, is driven by immune cells and cytokines. Recent evidence indicated that interleukin (IL)-27 showed pleiotropic properties in immune diseases. However, precise mechanisms of IL-27, especially in atherosclerosis remains unknown. In our research, we examined the influence of the administration of IL-27 and an anti-IL-27p28 antibody (anti-IL-27p28-Ab) on both the initiation and the progression of atherosclerosis. In the groups (both the initiation and the progression) receiving recombinant IL-27 administration, the formation of atherosclerotic plaques was suspended, and the percentage of regulatory T cells (LAP+ or Foxp3+) in the spleen and peripheral blood was increased. Meanwhile, the number of T helper 1 (Th1) and T helper 17 (Th17) cells was decreased. In the peripheral blood plasma, TGF-β and IL-10 expression were increased, while the levels of IFN-γ and IL-17 were reduced. As for lesions, the mRNA expression of Foxp3, TGF-β, and IL-10 was increased, while that of IFN-γ and IL-17 was reduced. In the anti-IL-27p28 antibody groups, we obtained opposite results. We also observed that DCs treated with IL-27 display a tolerogenic phenotype and that IL-27–treated tolerogenic DCs (tDCs) are likely to play a protective role during atherosclerosis. Our study indicates that IL-27 or adoptive transfer of IL-27 loaded tDCs may be a new therapeutic approach in atherosclerosis.
Published: 2022
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8. Circulating myocardial microRNAs from infarcted hearts are carried in exosomes and mobilise bone marrow progenitor cells

Author: Min Cheng, Junjie Yang, Xiaoqi Zhao, Eric Zhang, Qiutang Zeng, Yang Yu, Liu Yang, Bangwei Wu, Guiwen Yi, Xiaobo Mao, Kai Huang, Nianguo Dong, Min Xie, Nita A. Limdi, Sumanth D. Prabhu, Jianyi Zhang, and Gangjian Qin
Subjects: Science
Abstract: During myocardial infarction, microRNAs (myo-miRs) are released into the circulation. Here Cheng et al. show that myo-miRs carried in exosomes are transferred to the bone marrow (BM), downregulate expression of CXCR4 in mononuclear cells, and increase the number of circulating BM progenitor cells, thus orchestrating a systemic response to myocardial injury.
Published: 2019
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9. Corrigendum: Galectin-9: A Suppressor of Atherosclerosis?

Author: Jian Yu, Ruirui Zhu, Kunwu Yu, Yue Wang, Yan Ding, Yucheng Zhong, and Qiutang Zeng
Subjects: Galectin-9, atherosclerosis, T-cell immunoglobulin mucin 3, regulatory T cells, T helper cells, Immunologic diseases. Allergy, RC581-607
Published: 2021
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10. Galectin-9: A Suppressor of Atherosclerosis?

Author: Jian Yu, Ruirui Zhu, Kunwu Yu, Yue Wang, Yan Ding, Yucheng Zhong, and Qiutang Zeng
Subjects: Galectin-9, atherosclerosis, T-cell immunoglobulin mucin 3, regulatory T cells, T helper cells, Immunologic diseases. Allergy, RC581-607
Abstract: It is no longer controversial that atherosclerosis is a vascular wall chronic inflammatory disease mediated by cells of innate and adaptive immunity. Galectin-9 (Gal-9) seems to be a crucial regulator of T-cell immunity by inducing apoptosis in specific T-cell subpopulations associated with autoimmunity and inflammatory disease. Accumulating evidence showed that galectin-9 signaling via T-cell immunoglobulin mucin 3 (TIM-3) is concerned with different regulatory functions in autoimmunity, including direct depletion of pro-inflammatory T-cells, expanding the number of regulatory T cells, altering macrophages to an anti-inflammatory state and the induction of repressive myeloid-derived suppressor cells. In addition, anti-Tim-3-Ab administration increased atherosclerotic plaque formation by blocking Tim-3–galectin-9 interaction. Hence, we hypothesize that galectin-9 may be a novel therapy for atherosclerotic disease. Further researches are needed to investigate the precise effect of galectin-9 in the process of atherosclerosis.
Published: 2020
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11. Clinical Characteristics and Prognosis of 244 Cardiovascular Patients Suffering From Coronavirus Disease in Wuhan, China

Author: Yudong Peng, Kai Meng, Meian He, Ruirui Zhu, Hongquan Guan, Zihan Ke, Liang Leng, Xiang Wang, Bende Liu, Caiying Hu, Qingwei Ji, Mulatibieke Keerman, Longxian Cheng, Tangchun Wu, Kai Huang, and Qiutang Zeng
Subjects: cardiovascular disease, coronavirus disease, COVID‐19, respiratory failure, SARS‐CoV‐2, severe acute respiratory syndrome coronavirus 2, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract: Background The coronavirus disease 2019 (COVID‐19) has developed into a global outbreak. Patients with cardiovascular disease (CVD) with COVID‐19 have different clinical characteristics and prognostic outcomes. This study aimed to summarize the clinical characteristics and laboratory indicators of patients with COVID‐19 with CVD, especially the critically ill patients. Methods and Results This study included 244 patients diagnosed with COVID‐19 and CVD (hypertension, coronary heart disease, or heart failure). The patients were categorized into critical (n=36) and noncritical (n=208) groups according to the interim guidance of China’s National Health Commission. Clinical, laboratory, and outcome data were collected from the patients’ medical records and compared between the 2 groups. The average body mass index of patients was significantly higher in the critical group than in the noncritical group. Neutrophil/lymphocyte ratio, and C‐reactive protein, procalcitonin, and fibrinogen, and d‐dimer levels at admission were significantly increased in the critical group. The all‐cause mortality rate among cases of COVID‐19 combined with CVD was 19.26%; the proportion of coronary heart disease and heart failure was significantly higher in deceased patients than in recovered patients. High body mass index, previous history of coronary heart disease, lactic acid accumulation, and a decrease in the partial pressure of oxygen were associated with death. Conclusions All‐cause mortality in patients with COVID‐19 with CVD in hospitals is high. The high neutrophil/lymphocyte ratio may be a predictor of critical patients. Overweight/obesity combined with coronary heart disease, severe hypoxia, and lactic acid accumulation resulting from respiratory failure are related to poor outcomes. Registration URL: https://www.chictr.org.cn; Unique identifier: ChiCTR2000029865.
Published: 2020
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12. Heat Shock Protein 22 Attenuates Doxorubicin-Induced Cardiotoxicity via Regulating Inflammation and Apoptosis

Author: Yin Lan, Yi Wang, Kun Huang, and Qiutang Zeng
Subjects: doxorubicin, Hsp22, inflammation, apoptosis, TLR/NLRP3, Therapeutics. Pharmacology, RM1-950
Abstract: BackgroundThe antitumor effect of doxorubicin (DOX) is limited by its acute and chronic toxicity to the heart, which causes heart injury. Heat shock protein 22 (Hsp22) is a protein proved to exert anti-apoptosis and anti-inflammatory effects in other diseases and physical conditions. In this study, we aim to explore whether Hsp22 could exert a protective role during cardiac injury in response to DOX.MethodsThe overexpression of Hsp22 was mediated via adenovirus vector to clarify the role of Hsp22 in the cardiac injury caused by DOX. DOX-induced acute heart injury mouse model was established by single intraperitoneal injection of DOX (15 mg/kg). Subsequently, cardiac staining and molecular biological analysis were performed to analyze the morphological and biochemical effects of Hsp22 on cardiac injury. H9c2 cells were used for validation in vitro.ResultsAn increase in the expression level of Hsp22 was observed in DOX-treated heart tissue. Furthermore, cardiac-specific overexpression of Hsp22 showed reduced cardiac dysfunction, decrease in inflammatory response, and reduction in cell apoptosis in injury heart and cardiomyocytes induced by DOX in vivo and in vitro. Moreover, the suppression of Toll-like receptor (TLR)4/NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) was associated with the protective effect of Hsp22. Finally, the protective effect of Hsp22 cardiac function was almost abolished by overexpression of NLRP3 in DOX-treated mice.ConclusionIn summary, Hsp22 overexpression in the heart could suppress cardiac injury in response to DOX treatment through blocking TLR4/NLRP3 activation. Hsp22 may become a new therapeutic method for treating cardiac injury induced by DOX in cancer patients.
Published: 2020
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13. The IL-2/Anti-IL-2 Complex Attenuates Cardiac Ischaemia-Reperfusion Injury Through Expansion of Regulatory T Cells

Author: Junhui Xiao, Kunwu Yu, Ming Li, Chuanyin Xiong, Yuzhen Wei, and Qiutang Zeng
Subjects: Cytokines, Inflammation, Immunotherapy, Ischaemia/reperfusion injury, Regulatory T-lymphocytes (Tregs), Physiology, QP1-981, Biochemistry, QD415-436
Abstract: Background/Aims: Regulatory T cells (Tregs) can suppress immunologic damage in myocardial ischaemia/reperfusion injury (MIRI), however, the isolation and ex vivo expansion of these cells for clinical application remains challenging. Here, we investigated whether the IL-2/anti-IL-2 complex (IL-2C), a mediator of Treg expansion, can attenuate MIRI in mice. Methods: Myocardial I/R was surgically induced in male C57BL/6 mice, aged 8-10 weeks, that were randomly assigned to 1) sham group (Sham), 2) Phosphate Buffered Saline (PBS), 3) IL-2-anti-IL-2 Ab complex (IL-2C), or 4) sham group, 5) PBS, 6) IL-2C after MIRI, or 7) IL-2C, 8) IL-2C+anti-CD25 mAbs, or 9) IL-2C; 10) IL-2C+anti-TGF-β1 mAbs, 11) IL-2C+anti-IL-10 mAbs. The following parameters were measured at different time points: infarct area, myocardial apoptosis, splenocytes, the inhibitory function of Tregs, and presence of inflammatory factors. In addition, immunohistochemistry analysis was performed. Results: We observed that Tregs were activated in response to MIRI. IL-2C administered before MIRI induced Treg expansion in both spleen and heart, attenuated Th1 and Th17 cell numbers, improved myocardial function, and attenuated both infiltration of inflammatory cells and apoptosis after MIRI. Furthermore, IL-2C administration reduced expression of inflammatory cytokines in the heart and attenuated proliferation of splenic cells. Depletion of Tregs with anti-CD25 mAb abrogated the beneficial effects of IL-2C. However, IL-2C–mediated myocardial protection was not dependent on either IL-10 or TGF-β. In addition, IL-2C administration after MIRI did not reduce infarct area, but did improve myocardial function slightly and reduced myocardial fibrosis. Conclusion: Our results demonstrate that IL-2C–induced Treg expansion attenuates MIRI and improves myocardial recovery in vivo, suggesting that IL-2C is a promising therapeutic target for myocardial IRI.
Published: 2017
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14. Exogenous interleukin 37 ameliorates atherosclerosis via inducing the Treg response in ApoE-deficient mice

Author: Qingwei Ji, Kai Meng, Kunwu Yu, Song Huang, Ying Huang, Xiaohong Min, Yucheng Zhong, Bangwei Wu, Yuzhou Liu, Shaoping Nie, Jianwei Zhang, Yujie Zhou, and Qiutang Zeng
Subjects: Medicine, Science
Abstract: Abstract Our previous study indicated that interleukin (IL)-37 is involved in atherosclerosis. In the present study, Anterior tibial arteries were collected from diabetes patients and controls. A histopathological analysis showed that IL-37 was over-expressed in human atherosclerotic plaques. Many types of cells including macrophages, vascular smooth muscle cells (VSMCs), endothelial cells and T lymphocyte expressed IL-37 in human atherosclerotic plaques. ApoE−/− mice were divided into a control group and a recombinant human IL-37-treated group. The IL-37 treatment resulted in a significant decrease in macrophages and CD4+ T lymphocytes and a substantial increase in VSMCs and collagen in atherosclerotic plaques, resulting in a reduction in atherosclerotic plaque size. Furthermore, the IL-37 treatment modulated the CD4+ T lymphocyte activity, including a decrease in T helper cell type 1 (Th1) and Th17 cells and an increase in regulatory T (Treg) cells, and inhibited the maturity of dendritic cells both in vivo and in vitro. In addition, treatment with anti-IL-10 receptor monoclonal antibody abrogated the anti-atherosclerotic effects of IL-37. These data suggest that exogenous IL-37 ameliorates atherosclerosis via inducing the Treg response. IL-37 may be a novel therapeutic to prevent and treat atherosclerotic disease.
Published: 2017
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15. IL-37 Plays a Beneficial Role in Patients with Acute Coronary Syndrome

Author: Xiaobo Mao, Ruirui Zhu, Fangyuan Zhang, Yucheng Zhong, Kunwu Yu, Yuzhen Wei, Haitao Sun, Wenbin Xu, Quan Luo, Yue Wang, Yan Ding, and Qiutang Zeng
Subjects: Pathology, RB1-214
Abstract: Background. Interleukin-37 (IL-37) acts as an inhibitor of innate and adaptive immunity. However, the exact role of IL-37 in the patients with acute coronary syndrome (ACS) remains to be elucidated. Methods. Patients were classified into 4 groups: normal coronary artery (NCA), stable angina (SA), unstable angina (UA), and acute myocardial infarction (AMI). The circulating Treg, Th1, and Th17 frequencies were measured. The effect of IL-37 on stimulated peripheral blood mononuclear cells (PBMCs) and the influence of IL-37 on DCs were explored. In addition, the role of IL-37-treated tDCs on Treg cell expansion and the stability of these tDCs were also tested. Results. Our results showed that the circulating Treg frequencies were decreased, while Th1 and Th17 frequencies were increased in ACS patients, and that IL-37 expanded Tregs but suppressed Th1 and Th17 cells in activated PBMCs derived from ACS patients. Of note, IL-37-treated human DCs obtained a tolerogenic phenotype, and such tDCs promoted expansion of Tregs and decreased the Th1 and Th17 populations when cocultured with CD4+ T cells. Interestingly, IL-37-treated DCs from patients with ACS are phenotypically and functionally comparable to IL-37-treated DCs from NCA patients, and tolerogenic properties of IL-37-treated DCs were highly stable. Conclusion. In conclusion, our results reveal a beneficial role of IL-37 in the patients with ACS and suggest that autologous IL-37-treated tDCs may be a novel therapeutic strategy for the patients with ACS.
Published: 2019
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16. Heme Oxygenase-1 Restores Impaired GARP+CD4+CD25+ Regulatory T Cells from Patients with Acute Coronary Syndrome by Upregulating LAP and GARP Expression on Activated T Lymphocytes

Author: Yuzhou Liu, Xiaoqi Zhao, Yucheng Zhong, Kai Meng, Kunwu Yu, Huairui Shi, Bangwei Wu, Hasahya Tony, Jianghao Zhu, Ruirui Zhu, Yudong Peng, Yi Mao, Peng Cheng, Xiaobo Mao, and Qiutang Zeng
Subjects: Heme oxygenase-1, GARP+ CD4+ CD25+Tregs, LAP, Foxp3, Acute coronary syndrome, Physiology, QP1-981, Biochemistry, QD415-436
Abstract: Background: Accumulating evidence shows that the pathological autoreactive immune response is responsible for plaque rupture and the subsequent onset of acute coronary syndrome (ACS). Naturally occurring CD4+CD25+regulatory T cells (nTregs) are indispensable in suppressing the pathological autoreactive immune response and maintaining immune homeostasis. However, the number and the suppressive function of glycoprotein-A repetitions predominant (GARP) + CD4+ CD25+ activated nTregs were impaired in patients with ACS. Recent evidence suggests that heme oxygenase-1 (HO-1) can regulate the adaptive immune response by promoting the expression of Foxp3. We therefore hypothesized that HO-1 may enhance the function of GARP+ CD4+ CD25+Tregs in patients with ACS and thus regulate immune imbalance. Methods: T lymphocytes were isolated from healthy volunteers (control, n=30) and patients with stable angina (SA, n=40) or ACS (n=51). Half of these cells were treated with an HO-1 inducer (hemin) for 48 h, and the other half were incubated with complete RPMI-1640 medium. The frequencies of T-helper 1 (Th1), Th2, Th17 and latency-associated peptide (LAP) +CD4+ T cells and the expression of Foxp3 and GARP by CD4+CD25+T cells were then assessed by measuring flow cytometry after stimulation in vitro. The suppressive function of activated Tregs was measured by thymidine uptake. The levels of transforming growth factor-1 (TGF-β1) in the plasma were measured using enzyme-linked immunosorbent assay (ELISA). The expression levels of the genes encoding these proteins were analyzed by real-time polymerase chain reaction. Results: Patients with ACS exhibited an impaired number and suppressive function of GARP+ CD4+ CD25+Tregs and a mixed Th1/Th17-dominant T cell response when compared with the SA and control groups. The expression of LAP in T cells was also lower in patients with ACS compared to patients with SA and the control individuals. Treatment with an HO-1 inducer enhanced the biological activity of GARP+ CD4+ CD25+Tregs and resulted in increased expression of LAP and GARP by activated T cells. Conclusions: The reduced number and impaired suppressive function of GARP+ CD4+ CD25+Tregs result in excess effector T cell proliferation, leading to plaque instability and the onset of ACS. HO-1 can effectively restore impaired GARP+ CD4+ CD25+Tregs from patients with ACS by promoting LAP and GARP expression on activated T cells.
Published: 2015
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17. MicroRNA-101a Inhibits Cardiac Fibrosis Induced by Hypoxia via Targeting TGFβRI on Cardiac Fibroblasts

Author: Xin Zhao, Kejing Wang, Yuhua Liao, Qiutang Zeng, Yushu Li, Fen Hu, Yuzhou Liu, Kai Meng, Cheng Qian, Qing Zhang, Hongquan Guan, Kaige Feng, You Zhou, Yimei Du, and Zhijian Chen
Subjects: Cardiac fibrosis, Cardiac fibroblasts, Hypoxia, MicroRNAs, Transforming growth factor β receptor I, Physiology, QP1-981, Biochemistry, QD415-436
Abstract: Background/Aims: Hypoxia is a basic pathological challenge that is associated with numerous cardiovascular disorders including aberrant cardiac remodeling. Transforming growth factor beta (TGF-β) signaling pathway plays a pivotal role in mediating cardiac fibroblast (CF) function and cardiac fibrosis. Recent data suggested that microRNA-101a (miR-101a) exerted anti-fibrotic effects in post-infarct cardiac remodeling and improved cardiac function. This study aimed to investigate the potential relationship between hypoxia, miR-101a and TGF-β signaling pathway in CFs. Methods and Results: Two weeks following coronary artery occlusion in rats, the expression levels of both TGFβ1 and TGFβRI were increased, but the expression of miR-101a was decreased at the site of the infarct and along its border. Cultured rat neonatal CFs treated with hypoxia were characterized by the up-regulation of TGFβ1 and TGFβRI and the down-regulation of miR-101a. Delivery of miR-101a mimics significantly suppressed the expression of TGFβRI and p-Smad 3, CF differentiation and collagen content of CFs. These anti-fibrotic effects were abrogated by co-transfection with AMO-miR-101a, an antisense inhibitor of miR-101a. The repression of TGFβRI, a target of miR-101a, was validated by luciferase reporter assays targeting the 3'UTR of TGFβRI. Additionally, we found that overexpression of miR-101a reversed the improved migration ability of CFs and further reduced CF proliferation caused by hypoxia. Conclusion: Our study illustrates that miR-101a exerts anti-fibrotic effects by targeting TGFβRI, suggesting that miR-101a plays a multi-faceted role in modulating TGF-β signaling pathway and cardiac fibrosis.
Published: 2015
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18. Impairment of Circulating CD4+CD25+GARP+ Regulatory T Cells in Patients with Acute Coronary Syndrome

Author: Kai Meng, Wei Zhang, Yucheng Zhong, Xiaobo Mao, Yingzhong Lin, Ying Huang, Mingjian Lang, Yudong Peng, Zhengfeng Zhu, Yuzhou Liu, Xiaoqi Zhao, Kunwu Yu, Bangwei Wu, Qingwei Ji, and Qiutang Zeng
Subjects: Atherosclerosis, Regulatory T cells, GARP, Immune system, Acute coronary syndrome, Physiology, QP1-981, Biochemistry, QD415-436
Abstract: Background: Atherosclerosis (AS) is an inflammatory and immune disease. Regulatory T cells (Tregs) suppress the activation of T cells and have been shown to play a protective role during the pathogenesis of AS. However, specific markers for Tregs are lacking. Recently, glycoprotein A repetitions predominant (GARP) was discovered as a specific marker of activated Tregs, and we therefore utilized GARP as a specific surface marker for Tregs in the current study. Methods: To assess whether GARP+ Tregs are downregulated in patients with acute coronary syndrome (ACS), we examined CD4+CD25+GARP+ T cell frequencies as well as their associated cytokines and suppressive function. Additionally, we compared GARP expression to that of FOXP3, which may be more sensitive as a marker of activated Tregs in patients with ACS. Results: Patients with ACS demonstrated a significant decrease in circulating CD4+CD25+GARP+ Tregs. Moreover, the suppressive function of Tregs and levels of related cytokines were also impaired in ACS patients compared to those with stable angina (SA) or normal coronary artery (NCA). Additionally, after TCR stimulation, peripheral blood mononuclear cells (PBMCs) from patients with ACS exhibited a decrease in CD4+CD25+GARP+ Tregs. Conclusions: These fnding indicate that circulating CD4+CD25+GARP+ Tregs are impaired in patients withACS. Thus, targeting GARP may promote the protective function of Tregs in ACS.
Published: 2014
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19. Interleukin‐37 and Dendritic Cells Treated With Interleukin‐37 Plus Troponin I Ameliorate Cardiac Remodeling After Myocardial Infarction

Author: Ruirui Zhu, Haitao Sun, Kunwu Yu, Yucheng Zhong, Huairui Shi, Yuzhen Wei, Xin Su, Wenbin Xu, Quan Luo, Fangyuan Zhang, Zhengfeng Zhu, Kai Meng, Xiaoqi Zhao, Yuzhou Liu, Yi Mao, Peng Cheng, Xiaobo Mao, and Qiutang Zeng
Subjects: interleukin‐37, myocardial infarction, remodeling, tolerogenic dendritic cells, Treg cells, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract: BackgroundExcessive immune‐mediated inflammatory reactions play a deleterious role in postinfarction ventricular remodeling. Interleukin‐37 (IL‐37) emerges as an inhibitor of both innate and adaptive immunity. However, the exact role of IL‐37 and IL‐37 plus troponin I (TnI)–treated dendritic cells (DCs) in ventricular remodeling after myocardial infarction (MI) remains elusive. Methods and ResultsMI was induced by permanent ligation of the left anterior descending artery. Our results showed that treatment with recombinant human IL‐37 significantly ameliorated ventricular remodeling after MI, as demonstrated by decreased infarct size, better cardiac function, lower mortality, restricted inflammatory responses, decreased myocardial fibrosis, and inhibited cardiomyocyte apoptosis. In vitro, we examined the phenotype of IL‐37 plus TnI–conditioned DCs of male C57BL/6 mice and their capacity to influence the number of regulatory T cells. Our results revealed that IL‐37 plus TnI–conditioned DCs obtained the characteristics of tolerogenic DCs (tDCs) and expanded the number of regulatory T cells when co‐cultured with splenic CD4+ T cells. Interestingly, we also found that adoptive transfer of these antigen‐loaded tDCs markedly increased the number of regulatory T cells in the spleen, attenuated the infiltration of inflammatory cells in the infarct hearts, decreased myocardial fibrosis, and improved cardiac function. ConclusionsOur results reveal a beneficial role of IL‐37 or tDCs treated with IL‐37 plus TnI in post‐MI remodeling that is possibly mediated by reestablishing a tolerogenic immune response, indicating that IL‐37 or adoptive transfer of IL‐37 plus TnI–treated tDCs may be a novel therapeutic strategy for ventricular remodeling after MI.
Published: 2016
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20. Chemerin15-Ameliorated Cardiac Ischemia-Reperfusion Injury Is Associated with the Induction of Alternatively Activated Macrophages

Author: Chao Chang, Qingwei Ji, Bangwei Wu, Kunwu Yu, Qiutang Zeng, Shuanli Xin, Jixiang Liu, and Yujie Zhou
Subjects: Pathology, RB1-214
Abstract: Chemerin15 (C15), an endogenous anti-inflammatory component, inhibits the activity of neutrophils and macrophages through G protein-coupled receptor ChemR23; however, its role as well as functional mechanism in mouse myocardial ischemia/reperfusion (I/R) injury remains unknown. Methods. Sham or I/R operations were performed on C57BL/6J mice. The I/R mice received an injection of C15 immediately before reperfusion. Serum troponin T levels, infarct size, cardiomyocyte apoptosis, reactive oxygen species (ROS) production, and infiltration of neutrophils were assessed 24 h after reperfusion, while the macrophage phenotypes, macrophage infiltration, and inflammatory cytokine levels were assessed 48 h after reperfusion. Results. Compared with the control group, the C15-treated mice showed an obvious amelioration of I/R injury and displayed less ROS, accompanied by reduced neutrophil recruitment. C15 decreased the tumor necrosis factor- (TNF-) α and interleukin- (IL-) 6 levels and increased the IL-10 levels in the serum of the I/R mice, which suggested a suppressed inflammatory response that could be related to elevated alternatively activated M2 macrophages with characteristic skewed expression of M2 markers and inhibition of classically activated M1 marker expression. Conclusion. C15 may induce alternatively activated M2 macrophage polarization and suppress the inflammatory response to protect against myocardial I/R injury in mice.
Published: 2015
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21. MicroRNA-208a Dysregulates Apoptosis Genes Expression and Promotes Cardiomyocyte Apoptosis during Ischemia and Its Silencing Improves Cardiac Function after Myocardial Infarction

Author: Hasahya Tony, Kai Meng, Bangwei Wu, Aijia Yu, Qiutang Zeng, Kunwu Yu, and Yucheng Zhong
Subjects: Pathology, RB1-214
Abstract: Aims. miR-208a is associated with adverse outcomes in several cardiac pathologies known to have increased apoptosis, including myocardial infarction (MI). We investigated if miR-208a has proapoptotic effects on ischemic cardiomyocytes and if its silencing has therapeutic benefits in MI. Methods and Results. The effect of miR-208a on apoptosis during ischemia was studied in cultured neonatal mice myocytes transfected with agomir or antagomir. Differential gene expression was assessed using microarrays. MI was induced in male C57BL/6 mice randomly assigned to antagomir (n=6) or control group (n=7), while sham group (n=7) had sham operation done. Antagomir group received miR208a antagomir, while control and sham group mice received vehicle only. At 7 and 28 days, echocardiography was done and thereafter hearts were harvested for analysis of apoptosis by TUNEL method, fibrosis using Masson’s trichrome, and hypertrophy using hematoxylin and eosin. miR-208a altered apoptosis genes expression and increased apoptosis in ischemic cardiomyocytes. Therapeutic inhibition of miR-208a decreased cardiac fibrosis, hypertrophy, and apoptosis and significantly improved cardiac function 28 days after MI. Conclusion. miR-208a alters apoptosis genes expression and promotes apoptosis in ischemic cardiomyocytes, and its silencing attenuates apoptosis, fibrosis, and hypertrophy after MI, with significant improvement in cardiac function.
Published: 2015
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22. A Potential Mechanism of High-Dose Ticagrelor in Modulating Platelet Activity and Atherosclerosis Mediated by Thymic Stromal Lymphopoietin Receptor.

Author: Yi Mao, Yudong Peng, Qiutang Zeng, Longxian Cheng, Boyuan Wang, Xiaobo Mao, Kai Meng, Yuzhou Liu, Yitian Lian, and Dazhu Li
Subjects: Medicine, Science
Abstract: Abnormal expression of thymic stromal lymphopoietin (TSLP) and its receptor (TSLPR) was found in patients with acute coronary syndrome. Ticagrelor, an oral platelet ADP P2Y12 receptor antagonist, is widely used in these patients. The aim of this study was to verify whether different doses of ticagrelor regulated plaque progression and platelet activity by modulating TSLP/TSLPR. Seventy-five ApoE-/- mice were randomly divided into five groups: (1) high-cholesterol diet (HCD, n = 15); (2) HCD plus ticagrelor 25 mg/kg/d (T1, n = 15); (3) HCD plus ticagrelor 50 mg/kg/d (T2, n = 15); (4) HCD plus ticagrelor 100 mg/kg/d (T3, n = 15); and (5) a normal diet group (ND, n = 15). At day 0 and at week 16, blood lipids and serum TSLP levels, expression of TSLPR, CD62, and CD63, platelet aggregation, platelet ATP release, PI3K/Akt signaling pathway, and plaque morphology were assessed. HCD increased TSLPR expression and atherosclerosis progression but high-dose ticagrelor (100 mg/kg) moderated this trend. TSLPR was positively correlated with Akt1, platelet aggregation, corrected plaque area, and vulnerability index in the T3 group (P
Published: 2015
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23. Association of SNP Rs9943582 in APLNR with Left Ventricle Systolic Dysfunction in Patients with Coronary Artery Disease in a Chinese Han GeneID Population.

Author: Pengyun Wang, Chengqi Xu, Chuchu Wang, Yanxia Wu, Dan Wang, Shanshan Chen, Yuanyuan Zhao, Xiaojing Wang, Sisi Li, Qin Yang, Qiutang Zeng, Xin Tu, Yuhua Liao, Qing K Wang, and Xiang Cheng
Subjects: Medicine, Science
Abstract: Heart failure affects 1-2% of the adult population worldwide and coronary artery disease (CAD) is the underlying etiology of heart failure in 70% of the patients. The pathway of apelin and its apelin receptor (APJ) was implicated in the pathogenesis of heart failure in animal models, but a similar role in humans is unknown. We studied a functional variant, rs9943582 (-154G/A), at the 5'-untranslated region, that was associated with decreased expression of the APJ receptor gene (APLNR) in a population consisting of 1,751 CAD cases and 1,022 controls. Variant rs9943582 was not associated with CAD, but among CAD patients, it showed significant association with left ventricular systolic dysfunction (431 CAD patients with left ventricular systolic dysfunction (LV ejection fraction or LVEF< 40%) versus 1,046 CAD patients without LV systolic dysfunction (LVEF>50%) (P-adj = 6.71 × 10(-5), OR = 1.43, 95% CI, 1.20-1.70). Moreover, rs9943582 also showed significant association with quantitative echocardiographic parameters, including left ventricular end-diastolic diameter (effect size: increased 1.67 ± 0.43 mm per risk allele A, P = 1.15 × 10(-4)), left atrial size (effect size: increased 2.12 ± 0.61 mm per risk allele A, P = 9.56 × 10(-4)) and LVEF (effect size: decreased 2.59 ± 0.32 percent per risk allele A, P = 7.50 × 10(-15)). Our findings demonstrate that allele A of rs9943582 was significantly associated with left ventricular systolic dysfunction, left ventricular end-diastolic diameter, the left atrial diameter and LVEF in the CAD population, which suggests an important role of the apelin/APJ system in the pathology of heart failure associated with ischemic heart disease.
Published: 2015
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24. Atorvastatin Improves Inflammatory Response in Atherosclerosis by Upregulating the Expression of GARP

Author: Xiaoqi Zhao, Yuzhou Liu, Yucheng Zhong, Bo Liu, Kunwu Yu, Huairui Shi, Ruirui Zhu, Kai Meng, Wei Zhang, Bangwei Wu, and Qiutang Zeng
Subjects: Pathology, RB1-214
Abstract: Regulatory T cells play an important role in the progression of atherosclerosis. GARP is a newly biological membrane molecule existed on activated Tregs, which is related to the release of TGF-β. The antiatherosclerosis effects of statins partly depend on their multiple immune modulatory potencies. In this paper, we present that atorvastatin could upregulate the expression of GARP and TGF-β in CD4+ T cells and increase the numbers of CD4+LAP+ and CD4+Foxp3+ regulatory T cells in ApoE−/− mice. Also, we indicate that atorvastatin promotes the aggregation of GARP+ and Foxp3+ cells and secretory of the TGF-β1 in atherosclerotic plaques. Furthermore, we prove that atorvastatin could delay the procession of atherosclerosis and improve the stability of atherosclerotic plaques. Interestingly, we report that inhibition of GARP distinctly inhibits the anti-inflammatory effects of atorvastatin. We conclude that atorvastatin improves the inflammatory response in atherosclerosis partly by upregulating the expression of GARP on regulatory T cells.
Published: 2015
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25. Elevated Plasma IL-38 Concentrations in Patients with Acute ST-Segment Elevation Myocardial Infarction and Their Dynamics after Reperfusion Treatment

Author: Yucheng Zhong, Kunwu Yu, Xiang Wang, Xiaoya Wang, Qingwei Ji, and Qiutang Zeng
Subjects: Pathology, RB1-214
Abstract: Objective. Recent studies suggest that IL-38 is associated with autoimmune diseases. Furthermore, IL-38 is expressed in human atheromatous plaque. However, the plasma levels of IL-38 in patients with ST-segment elevation myocardial infarction (STEMI) have not yet to be investigated. Methods. On admission, at 24 h, at 48 h, and at 7 days, plasma IL-38, C-reactive protein (CRP), cardiac troponin I (cTNI), and N-terminal of the prohormone brain natriuretic peptide (NT-proBNP) levels were measured and IL-38 gene in peripheral blood mononuclear cells (PBMCs) was detected in STEMI patients. Results. The results showed that plasma IL-38 levels and IL-38 gene expression in PBMCs were significantly increased in STEMI patients compared with control group and were time dependent, peaked at 24 h. In addition, plasma IL-38 levels were dramatically reduced in patients with reperfusion treatment compared with control group. Similar results were also demonstrated with CRP, cTNI, and NT-proBNP levels. Furthermore, IL-38 levels were found to be positively correlated with CRP, cTNI, and NT-proBNP and be weakly negatively correlated with left ventricular ejection fraction (LVEF) in STEMI patients. Conclusions. The results indicate that circulating IL-38 is a potentially novel biomarker for patients with STEMI and IL-38 might be a new target for MI study.
Published: 2015
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26. Serum Galectin-9 Levels Are Associated with Coronary Artery Disease in Chinese Individuals

Author: Ruirui Zhu, Cheng Liu, Hongxia Tang, Qiutang Zeng, Xiang Wang, Zhengfeng Zhu, Yuzhou Liu, Xiaobo Mao, and Yucheng Zhong
Subjects: Pathology, RB1-214
Abstract: Background. Recently, several studies suggest that galectin-9 (Gal-9) might play a pivotal role in the pathogenesis of autoimmune diseases. However, the exact role of Gal-9 in atherosclerosis remains to be elucidated. Methods. Serum Gal-9, high-sensitivity C-reactive protein (hs-CRP), interferon- (IFN-) γ, interleukin- (IL-) 4, IL-17, and transforming growth factor- (TGF-) β1 were measured. The effect of Gal-9 on peripheral blood mononuclear cells (PBMC) was investigated in patients with normal coronary artery (NCA). Results. The lowest level of Gal-9 was found in the ST-segment elevation myocardial infarction (STEMI) group, followed by the non-ST-segment elevation ACS (NSTEACS), the NCA, and the stable angina pectoris (SAP) groups, respectively. Additionally, Gal-9 was found to be independently associated with hs-CRP, lipoprotein(a), and creatinine. Notably, Gal-9 was also noted to be an independent predictor of the Gensini score. Moreover, Gal-9 suppressed T-helper 17 (Th17) and expanded regulatory T cells (Tregs), resulting in decreased IL-17 production and increased secretion of TGF-β1. Conclusions. Serum Gal-9 is associated with not only coronary artery disease (CAD), but also the severity of coronary arteries stenosis. Gal-9 can expand Tregs and suppress Th17 development in activated PBMC, implying that Gal-9 has the potential to dampen the development of atherosclerosis and may be a new therapy for CAD.
Published: 2015
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27. Among Ectasia Patients with Coexisting Coronary Artery Disease, TIMI Frame Count Correlates with Ectasia Size and Markis Type IV Is the Commonest

Author: Hasahya Tony, Kai Meng, Bangwei Wu, and Qiutang Zeng
Subjects: Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract: Background. Coronary artery ectasia (CAE) occurs in 0.3 to 5.3% of patients undergoing coronary angiography. TIMI frame count (TFC) is an index of coronary flow that correlates with flow velocity. In ectasia patients, there is delayed coronary flow with increased TFC. Methods. We evaluated angiograms of 789 patients for presence of CAE, coronary artery disease (CAD), and Markis type of CAE. We measured ectasia size and length and their correlation with TFC in ectatic right coronary arteries (RCA) of patients with CAE and CAD. Results. 30 patients had CAE (3.8%). Of these 16.7% had isolated CAE, while 83.87% had CAE and CAD. Among CAE and CAD patients, the RCA was most involved (70.4%), and Markis type IV CAE was the commonest (64%). In isolated CAE, the RCA, LAD, and LCx were equally involved (33.3%). Patients with CAE and CAD had significantly higher TFC compared to controls, P=0.035. There was a positive correlation of moderate strength, between ectasia size and TFC, r(17) = 0.598, P=0.007. Ectasia length was not significantly correlated with TFC, rho (17) = 0.334, P=0.163. Conclusion. Among patients undergoing angiography, CAE has a prevalence of 3.8% and Markis type IV is the commonest. Larger ectasias are associated with slower coronary flow.
Published: 2015
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28. Autoantibodies Targeting AT1 Receptor from Patients with Acute Coronary Syndrome Upregulate Proinflammatory Cytokines Expression in Endothelial Cells Involving NF-κB Pathway

Author: Weijuan Li, Zhi Li, Yaoqi Chen, Songhai Li, Yuanyuan Lv, Wenping Zhou, Mengyang Liao, Feng Zhu, Zihua Zhou, Xiang Cheng, Qiutang Zeng, Yuhua Liao, and Yumiao Wei
Subjects: Immunologic diseases. Allergy, RC581-607
Abstract: Our study intended to prove whether agonistic autoantibodies to angiotensin II type 1 receptor (AT1-AAs) exist in patients with coronary heart disease (CHD) and affect the human endothelial cell (HEC) by upregulating proinflammatory cytokines expression involved in NF-κB pathway. Antibodies were determined by chronotropic responses of cultured neonatal rat cardiomyocytes coupled with receptor-specific antagonists (valsartan and AT1-EC2) as described previously. Interleukin-6 (IL-6), vascular cell adhesion molecule-1 (VCAM-1), and monocyte chemotactic protein-1 (MCP-1) expression were improved at both mRNA and protein levels in HEC, while NF-κB in the DNA level was improved detected by electrophoretic mobility shift assays (EMSA). These improvements could be inhibited by specific AT1 receptor blocker valsartan, NF-κB blocker pyrrolidine dithiocarbamate (PDTC), and specific short peptides from the second extracellular loop of AT1 receptor. These results suggested that AT1-AAs, via the AT1 receptor, induce expression of proinflammatory cytokines involved in the activation of NF-κB. AT1-AAs may play a great role in the pathogenesis of the acute coronary syndrome by mediating vascular inflammatory effects involved in the NF-κB pathway.
Published: 2014
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29. Elevated Plasma IL-37, IL-18, and IL-18BP Concentrations in Patients with Acute Coronary Syndrome

Author: Qingwei Ji, Qiutang Zeng, Ying Huang, Ying Shi, Yingzhong Lin, Zhengde Lu, Kai Meng, Bangwei Wu, Kunwu Yu, Meng Chai, Yuyang Liu, and Yujie Zhou
Subjects: Pathology, RB1-214
Abstract: Objective. More recently, evidence showed that the novel anti-inflammatory cytokine interleukin- (IL-) 37 was expressed in the foam-like cells of atherosclerotic coronary and carotid artery plaques, suggesting that IL-37 is involved in atherosclerosis-related diseases. However, the plasma levels of IL-37 in patients with acute coronary syndrome (ACS, including unstable angina pectoris and acute myocardial infarction) have yet to be investigated. Methods. Plasma IL-37, IL-18, and IL-18BP levels were measured in 50 patients with stable angina pectoris (SAP), 75 patients with unstable angina pectoris (UAP), 67 patients with acute myocardial infarction (AMI), and 65 control patients. Results. The plasma IL-37, IL-18, and IL-18BP levels were significantly increased in ACS patients compared to SAP and control patients. A correlation analysis showed that the plasma biomarker levels were positively correlated with each other and with the levels of C-reactive protein (CRP), N-terminal probrain natriuretic peptide (NT-proBNP), and left ventricular end-diastolic dimension (LVEDD) but negatively correlated with left ventricular ejection fraction (LVEF). Furthermore, the plasma IL-37, IL-18, and IL-18BP had no correlation with the severity of the coronary artery stenosis. Conclusions. The results indicate that the plasma IL-37 levels are associated with the onset of ACS.
Published: 2014
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30. Decreased plasma IL-35 levels are related to the left ventricular ejection fraction in coronary artery diseases.

Author: Yingzhong Lin, Ying Huang, Zhengde Lu, Cheng Luo, Ying shi, Qiutang Zeng, Yifeng Cao, Lin Liu, Xiaoyan Wang, and Qingwei Ji
Subjects: Medicine, Science
Abstract: BACKGROUND: Accumulating evidence shows that the novel anti-inflammatory cytokine IL-35 can efficiently suppress effector T cell activity and alter the progression of inflammatory and autoimmune diseases. The two subunits of IL-35, EBI3 and p35, are strongly expressed in human advanced plaque, suggesting a potential role of IL-35 in atherosclerosis and coronary artery disease (CAD). However, the plasma levels of IL-35 in patients with CAD have yet to be investigated. METHODS: Plasma IL-35, IL-10, TGF-β1, IL-12 and IL-27 levels were measured using an ELISA in 43 stable angina pectoris (SAP) patients, 62 unstable angina pectoris (UAP) patients, 56 acute myocardial infarction (AMI) patients and 47 chest pain syndrome patients as a control group. RESULTS: The results showed that plasma IL-35 levels were significantly decreased in the SAP group (90.74±34.22 pg/ml), the UAP group (72.20±26.63 pg/ml), and the AMI group (50.21±24.69 pg/ml) compared with chest pain syndrome group (115.06±32.27 pg/ml). Similar results were also demonstrated with IL-10 and TGF-β1. Plasma IL-12 and IL-27 levels were significantly increased in the UAP group (349.72±85.22 pg/ml, 101.75±51.42 pg/ml, respectively) and the AMI group (318.05±86.82 pg/ml, 148.88±68.45 pg/ml, respectively) compared with chest pain syndrome group (138.68±34.37 pg/ml, 63.60±22.75 pg/ml, respectively) and the SAP group (153.84±53.86 pg/ml, 70.84±38.77 pg/ml, respectively). Furthermore, lower IL-35 levels were moderately positively correlated with left ventricular ejection fraction (LVEF) in CAD patients (R = 0.416, P
Published: 2012
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31. A Randomized Comparison of 2 Different Drug-Coated Balloons for In-Stent Restenosis

Author: Shengwen Liu, Yujie Zhou, Zhujun Shen, Hui Chen, Chunguang Qiu, Guosheng Fu, Hui Li, Zaixin Yu, Qiutang Zeng, Zhanquan Li, Wei Li, and Shubin Qiao
Subjects: Cardiology and Cardiovascular Medicine
Published: 2023

32. Initial Invasive or Conservative Strategy for Stable Coronary Disease

Author: Maron D. J., Hochman J. S., Reynolds H. R., Bangalore S., O'Brien S. M., Boden W. E., Chaitman B. R., Senior R., Lopez-Sendon J., Alexander K. P., Lopes R. D., Shaw L. J., Berger J. S., Newman J. D., Sidhu M. S., Goodman S. G., Ruzyllo W., Gosselin G., Maggioni A. P., White H. D., Bhargava B., Min J. K., John Mancini G. B., Berman D. S., Picard M. H., Kwong R. Y., Ali Z. A., Mark D. B., Spertus J. A., Krishnan M. N., Elghamaz A., Moorthy N., Hueb W. A., Demkow M., Mavromatis K., Bockeria O., Peteiro J., Miller T. D., Szwed H., Doerr R., Keltai M., Selvanayagam J. B., Gabriel Steg P., Held C., Kohsaka S., Mavromichalis S., Kirby R., Jeffries N. O., Harrell F. E., Rockhold F. W., Broderick S., Bruce Ferguson T., Williams D. O., Harrington R. A., Stone G. W., Rosenberg Y, ISCHEMIA Research Group: Joseph Ricci, A Tello Montoliu, A I Robero Aniorte, Abbey Mulder, Abhay A Laddu, Abhinav Goyal, Abhishek Dubey, Abhishek Goyal, Abigail Knighton, Abraham Oomman, Adam J Jaskowiak, Adam Kolodziej, Adam Witkowski, Adnan Hameed, Adriana Anesini, Afshan Hussain, Agne Juceviciene, Agne Urboniene, Agnes Jakal, Agnieszka Szramowska, Ahmad Khairuddin, Ahmed Abdel-Latif, Ahmed Adel, Ahmed Aljzeeri, Ahmed Kamal, Ahmed Talaat, Aimee Mann, Aira Contreras, Ajit Kumar, V K Kumar, Akemi Furukawa, Akshay Bagai, Akvile Smigelskaite, Alain Furber, Alain Rheault, Alaine Melanie Loehr, Alan Rosen, Albert Varga, Albertina Qelaj, Alberto Barioli, Aldo Russo, Alec Moorman, Alejandro Gisbert, Aleksandra Fratczak, Aleksandras Laucevicius, Alena Kuleshova, Alessandro Sionis, Alexander A Sirker, Alexander M Chernyavskiy, Alexandra Craft, Alexandra Vazquez, Alexandre Ciappina Hueb, Alexandre S Colafranseschi, Alexandre Schaan de Quadros, Alexandre Tognon, Ali Alghamdi, Alice Manica Muller, Aline Nogueira Rabaça, Aline Peixoto Deiro, Alison Hallam, Allegra Stone, Allison Schley, Almudena Castro, Alvaro Rabelo Ales, Amanda Germann, Amanda O'Malley, Amar Uxa, Amarachi Ojajuni, Amarino C Oliveira Jr, Amber B Hull, Ambuj Roy, Amer Zarka, Amir Janmohamed, Ammani Brown, Ammy Malinay, Amparo Martinez Monzonis, Amy J Richards, Amy Iskandrian, Amy Ollinger, Ana D Djordjevic-Dikic, Ana Fernández Martínez, Ana Gomes Almeida, Ana Paula Batista, Ana Rita Francisco, Ana S Mladenovic, Ana Santana, Anam Siddiqui, Anastasia M Kuzmina-Krutetskaya, Andras Vertes, Andre S Sousa, Andre Gabriel, André Schmidt, Andrea M Lundeen, Andrea Bartykowszki, Andrea Lorimer, Andrea Mortara, Andrea Pascual, Andreia Coelho, Andreia Rocha, Andrés García-Rincón, Andrew G Howarth, Andrew J Moriarty, Andrew Docherty, Andrew Starovoytov, Andrew Zurick, Andrzej Łabyk, Andrzej Swiatkowski, Andy Lam, Anelise Kawakami, Angela Hoye, Angela Kim, Angelique Smit, Angelo Nobre, Anil V Shah, Anja Ljubez, Anjali Anand, Ankush Sachdeva, Ann Greenberg, Ann Luyten, Ann Ostrander, Anna Di Donato, Anna Cichocka-Radwan, Anna Fojt, Anna Plachcinska, Anna Proietti, Anna Teresinska, Anne Marie Webb, Anne Cartwright, Anne Heath, Anne Mackin, Anong Amaritakomol, Anong Chaiyasri, Anoop Chauhan, Anoop Mathew, Anthony Gemignani, Anto Luigi Andres, Antonia Vega, Antonietta Hansen, Antonino Ginel Iglesias, Antonio Carlos Carvalho, Antonio Di Chiara, Antonio Serra Peñaranda, Antonio Carvalho, Antonio Colombo, Antonio Fiarresga, Anupama Rao, Aquiles Valdespino-Estrada, Araceli Boan, Areef Ishani, Ariel Diaz, Arijit Ghosh, Arintaya Prommintikul, Arline Roberts, Arnold H Seto, Arnold P Good, Arshed Quyyumi, Arthur J Labovitz, Arthur Kerner, Arturo S Campos-Santaolalla, Arunima Misra, Ashok Mukherjee, Ashok Seth, Ashraf Seedhom, Asim N Cheema, Asker Ahmed, Atul Mathur, Atul Verma, Audrey W Leong, Axel Åkerblom, Axelle Fuentes, Aynun Naher, Badhma Valaiyapathi, Baljeet Kaur, Bandula Guruge, Barbara Brzezińska, Barbara Nardi, Bartosz Czarniak, Bebek Singh, Begoña Igual, Bela Merkely, Belen Cid Alvarez, Benjamin J Spooner, Benjamin J W Chow, Benjamin Cheong, Benoy N Shah, Bernard de Bruyne, Bernardas Valecka, Bernhard Jäger, Beth A Archer, Beth Abramson, Beth Jorgenson, Bethany Harvey, Betsy O'Neal, Bev Atkinson, Bev Bozek, Bevin Lang, Bijulal Sasidharan, Bin Yang, Bin Zhang, Binoy Mannekkattukudy Kurian, Bjoern Goebel, Bob Hu, Bogdan A Popescu, Bogdan Crnokrak, Bolin Zhu, Bonnie J Kirby, Brandi D Zimbelman, Brandy Starks, Branko D Beleslin, Brenda Hart, Brian P Shapiro, Brian McCandless, Brianna Wisniewski, Brigham R Smith, Brooks Mirrer, Bruce McManus, Bruce Rutkin, Bruna Edilena Paulino, Bruna Maria Ascoli, Bryn Smith, Byron J Allen, C Michael Gibson, C Noel Bairey Merz, Calin Pop, Cameron Hague, Camila Thais de Ormundo, Candace Gopaul, Candice P Edillo, Carísi A Polanczyk, Carita Krannila, Carla Vicente, Carl-Éric Gagné, Carlo Briguori, Carlos Peña Gil, Carlos Alvarez, Carly Ohmart, Carmen C Beladan, Carmen Ginghina, Carol M Kartje, Caroline Alsweiler, Caroline Brown, Caroline Callison, Caroline Pinheiro, Caroline Rodgers, Caroline Spindler, Carolyn Corbett, Carrie Drum, Casey Riedberger, Catherine Bone, Catherine Fleming, Catherine Gordon, Catherine Jahrsdorfer, Catherine Lemay, Catherine Weick, Cathrine Patten, Cecilia Goletto, Cezary Kepka, Chandini Suvarna, Chang Xu, Chantale Mercure, Charle A Viljoen, Charlene Wiyarand, Charles Jia-Yin Hou, Charles Y Lui, Charles Cannan, Charles Cornet, Charlotte Pirro, Chataroon Rimsukcharoenchai, Chen Wang, Cheng-Ting Tsai, Chen-Yen Chien, Cheryl A Allardyce, Chester M Hedgepeth, Chetan Patel, Chiara Attanasio, Chih-Hsuan Yen, Chi-Ming Chow, Ching Min Er, Ching-Ching Ong, Cholenahally Nanjappa Manjunath, Chris Beck, Chris Buller, Christel Vassaliere, Christian Hamm, Christiano Caldeira, Christie Ballantyne, Christina Björklund, Christine R Hinton, Christine Bergeron, Christine Masson, Christine Roraff, Christine Shelley, Christophe Laure, Christophe Thuaire, Christopher Kinsey, Christopher McFarren, Christopher Spizzieri, Christopher Travill, Chun-Chieh Liu, Chung-Lieh Hung, Chunguang Li, Chun-Ho Yun, Chunli Xia, Ciarra Heard, Cidney Schultz, Clare Venn-Edmonds, Claudia P Hochberg, Claudia Wegmayr, Claudia Cortés, Claudia Escobar, Cláudia Freixo, Claudio T Mesquita, Clemens T Kadalie, Colin Berry, Constance Philander, Corine Thobois, Costantino Costantini, Courtney Page, Craig Atkinson, Craig Barr, Craig Paterson, Cristina Bare, Cynthia Baumann, Cynthia Burman, Dalisa Espinosa, Damien Collison, Dan Deleanu, Dan Elian, Dan Gao, Dana Oliver, Daniel P Vezina, Daniel O'Rourke, Daniele Komar, Danielle Schade, Darrel P Francis, Dastan Malaev, David A Bull, David E Winchester, David P Faxon, David Booth, David Cohen, David DeMets, David Foo, David Schlichting, David Taggart, David Waters, David Wohns, Davis Vo, Dawid Teodorczyk, Dawn Shelstad, Dawn Turnbull, Dayuan Li, Dean Kereiakes, Deborah O'Neill, Deborah Yip, Debra K Johnson, Debra Dees, Deepak L Bhatt, Deepika Gopal, Deepti Kumar, Deirdre Mattina, Deirdre Murphy, Delano R Small, Delsa K Rose, Dengke Jiang, Denis Carl Phaneuf, Denise Braganza, Denise Fine, Derek Cyr, Desiree Tobin, Diana Cukali, Diana Parra, Diane Camara, Diane Minshall Liu, Diego Adrián Vences, Diego Franca de Cunha, Dimitrios Stournaras, Dipti Patel, Dongze Li, Donna Exley, Dorit Grahl, Dragana Stanojevic, Duarte Cacela, Dwayne S G Conway, E Pinar Bermudez, Eapen Punnoose, Edgar L Tay, Edgar Karanjah, Edoardo Verna, Eduardo Hernandez-Rangel, Edward D Nicol, Edward O McFalls, Edward T Martin, Edyta Kaczmarska, Ekaterina I Lubinskaya, Elena A Demchenko, Elena Refoyo Salicio, Eli Feen, Elihú Durán-Cortés, Elisabeth M Janzen, Elise L Hannemann, Elise van Dongen, Elissa Restelli Piloto, Eliza Kaplan, Elizabeta Srbinovska Kostovska, Elizabeth Capasso-Gulve, Elizabeth Congdon, Elizabeth Ferguson, Elizaveta V Zbyshevskaya, Ellen Magedanz, Ellie Fridell, Ellis W Lader, Elvin Kedhi, Emanuela Racca, Emilie Tachot, Emily DeRosa, Encarnación Alonso-Álvarez, Eric Nicollet, Eric Peterson, Erick Alexánderson Rosas, Erick Donato Morales, Erin Orvis, Ermina Moga, Estelle Montpetit, Estevao Figueiredo, Eugene Passamani, Eugenia Nikolsky, Eunice Yeoh, Evgeniy I Kretov, Ewa Szczerba, Ewelina Wojtala, Expedito Eustáquio Ribeiro Silva, F Marin Ortuño, Fabio R Farias, Fabio Fimiani, Fabrizio Rolfo, Fa-Chang Yu, Fadi Hage, Fadi Matar, Fahim Haider Jafary, Fang Feng, Fang Liu, Fatima Ranjbaran, Fatima Rodriguez, Fausto J Pinto, Fauzia Rashid, Federica Ramani, Fei Wang, Fernanda Igansi, Filipa Silva, Filippo Ottani, Fiona Haines, Firas Al Solaiman, Flávia Egydio, Flavio Lyra, Florian Egger, Fran Farquharson, Frances Laube, Francesc Carreras Costa, Francesca de Micco, Francesca Bianchini, Francesca Pezzetta, Francesca Pietrucci, Francesco Orso, Francesco Pisano, Francis Burt, Francisca Patuleia Figueiras, Francisco Fernandez-Aviles, Francois Pierre 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S.G., Ruzyllo W., Gosselin G., Maggioni A.P., White H.D., Bhargava B., Min J.K., John Mancini G.B., Berman D.S., Picard M.H., Kwong R.Y., Ali Z.A., Mark D.B., Spertus J.A., Krishnan M.N., Elghamaz A., Moorthy N., Hueb W.A., Demkow M., Mavromatis K., Bockeria O., Peteiro J., Miller T.D., Szwed H., Doerr R., Keltai M., Selvanayagam J.B., Gabriel Steg P., Held C., Kohsaka S., Mavromichalis S., Kirby R., Jeffries N.O., Harrell F.E., Rockhold F.W., Broderick S., Bruce Ferguson T., Williams D.O., Harrington R.A., Stone G.W., Rosenberg Y, and ISCHEMIA Research Group: Joseph Ricci, A Tello Montoliu, A I Robero Aniorte, Abbey Mulder, Abhay A Laddu, Abhinav Goyal, Abhishek Dubey, Abhishek Goyal, Abigail Knighton, Abraham Oomman, Adam J Jaskowiak, Adam Kolodziej, Adam Witkowski, Adnan Hameed, Adriana Anesini, Afshan Hussain, Agne Juceviciene, Agne Urboniene, Agnes Jakal, Agnieszka Szramowska, Ahmad Khairuddin, Ahmed Abdel-Latif, Ahmed Adel, Ahmed Aljzeeri, Ahmed Kamal, Ahmed Talaat, Aimee Mann, 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Bermudez, Eapen Punnoose, Edgar L Tay, Edgar Karanjah, Edoardo Verna, Eduardo Hernandez-Rangel, Edward D Nicol, Edward O McFalls, Edward T Martin, Edyta Kaczmarska, Ekaterina I Lubinskaya, Elena A Demchenko, Elena Refoyo Salicio, Eli Feen, Elihú Durán-Cortés, Elisabeth M Janzen, Elise L Hannemann, Elise van Dongen, Elissa Restelli Piloto, Eliza Kaplan, Elizabeta Srbinovska Kostovska, Elizabeth Capasso-Gulve, Elizabeth Congdon, Elizabeth Ferguson, Elizaveta V Zbyshevskaya, Ellen Magedanz, Ellie Fridell, Ellis W Lader, Elvin Kedhi, Emanuela Racca, Emilie Tachot, Emily DeRosa, Encarnación Alonso-Álvarez, Eric Nicollet, Eric Peterson, Erick Alexánderson Rosas, Erick Donato Morales, Erin Orvis, Ermina Moga, Estelle Montpetit, Estevao Figueiredo, Eugene Passamani, Eugenia Nikolsky, Eunice Yeoh, Evgeniy I Kretov, Ewa Szczerba, Ewelina Wojtala, Expedito Eustáquio Ribeiro Silva, F Marin Ortuño, Fabio R Farias, Fabio Fimiani, Fabrizio Rolfo, Fa-Chang Yu, Fadi Hage, Fadi Matar, Fahim Haider 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Niedzwiecka, J David Knight, Jacek Kusmierek, Jackie M White, Jackie Chow, Jacob Udell, Jacqueline E Tamis-Holland, Jacqueline Fannon, Jacquelyn A Quin, Jacquelyn Do, Jaekyeong Heo, Jakub Maksym, James E Davies, James H O'Keefe Jr, James J Jang, James Cha, James Harrison, James Hirsch, James Stafford, James Tatoulis, Jamie Rankin, Jan Henzel, Jan Orga, Jana Tancredi, Janaina Oliveira, Jane Burton, Jane Eckstein, Jane Marucci, Janet P Knight, Janet Blount, Janet Halliday, Janetta Kourzenkova, Janitha Raj, Jan-Malte Sinning, Jaqueline Pozzibon, Jaroslaw Drozdz, Jaroslaw Karwowski, Jason D Glover, Jason Loh Kwok, Jason T Call, Jason Linefsky, Jassira Gomes, Jati Anumpa, Javier J Garcia, Javier Courtis, Jay Meisner, K Jayakumar, Jayne Scales, Jean E Denaro, Jean Michel Juliard, Jean Ho, Jeanette K Stansborough, Jean-Michel Juliard, Jeanne Russo, Jeannette J M Schoep, Jeet Thambyrajah, Jeff Leimberger, Jeffery A Breall, Jeffrey A Kohn, Jeffrey C Milliken, Jeffrey Anderson, Jeffrey Blume, 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Wlodarczyk, Michel G Khouri, Michel S Slama, Michele Rawlins, Michelle M Bonner, Michelle M Seib, Michelle Chang, Michelle Crowder, Michelle Dixon, Michelle Mayon, Michelle McEvoy, Michelle Yee, Miguel M Fernandes, Miguel Nobre Menezes, Miguel Souto Bayarri, Miguel Barrero, Mikhail T Torosoff, Milan R Dobric, Milan Dobric, Milica Nikola Dekleva, Milind Avdhoot Gadkari, Millie Gomez, Min Tun Kyaw, Miriam Brooks, Miroslav Stevo Martinovic, Mitchel B Lustre, Mohammad Tariq Vakani, Mohammad El-Hajjar, Mohammed Al-Amoodi, Mohammed Hussain, Mohammed Saleem, Moisés Blanco-Calvo, Moisés Jiménez-Santos, Mona Bhatia, Monica Rosca, Monika Laukyte, Montserrat Gracida Blanca, Montserrat Vila Perales, Mouaz H Al-Mallah, Moysés de Oliveira Filho, Mpiko Ntsekhe, Muhamed Saric, Mulei Chen, Myriam Brousseau, Myrthes Emy Takiuti, Nada Cemerlic-Adjic, Nadia Asif, Nadia Gakou, Nafisa Hussain, Nana O Katamadze, Nancy L Clapp, Nancy Aedy, Nandita Nataraj, Nanette K Wenger, Naomi Uchida, Nasrul Ismail, Natalia S Oliveira, Natalia de Carvalho Maffei, Natalie Spitzer, Natasha C Putnam, Naved Aslam, Neamat Mowafy, Neeraj Pandit, Neeraj Parakh, Nevena Garcevic, Ngaire Meadows, Nhi N Tran, Nicholas Danchin, Nicki Lakeman, Nicola Johnston, Nicolas W Shammas, Nicole Saint Vrestil, Nicole Deming, Nier Zhong, Niket Patel, Nikola N Boskovic, Nikolaos Karogiannis, Nikos Werner, Nina Johnston, Ning Zhang, Ning Zhou, Niree Hindoyan, Nirmal Kumar, Nitika Chadha, Nitish Naik, Nodira Aripova, Noloyiso Mtana, Nona A Eskelson, Noor Syamira Mokhtar, Noppon Taksaudom, Nor Asiah Basri, Nora Marchelletta, Norma Hogg, Nungshi Jungla, Nuno Ferreira, Oksana A Lubyanaya, Olga B Nikolaeva, Olga Cañavate, Olga Sobrino, Olga Walesiak, Olga Walter, Olga Zdończyk, Olivia J Lim, Olivia Anaya, Olivia Mancilla, Olivier Dubourg, Olugbenga Bello, Omar Almousalli, Omar Thompson, Oni Olurinde, Or Harel, Osama Raheem, Oscar Méndiz, Óscar Prada-Delgado, Oz Shapira, P Christian Schulze, Pachara Panpunuan, Pal Maurovich-Horvat, Pallav Garg, Paloma Moraga, Pam Singh, Pamela Julian, Pamela Ouyang, Pamela Sigel, Pamela Woodard, Panpan Zhou, Paola Emanuela Poggio, Paola Smanio, Paolo Calabro, Paramjit Jeetley, Pascal Goube, Patricia K Nguyen, Patricia Alarie, Patricia Arakelian, Patricia Arsenault, Patricia Blaise, Patricia Brito, Patricia Cowper, Patricia Endsley, Patricia Mieses, Patrick B Alexander, Patrick Donnelly, Patrick Wilmot, Patrycja Lebioda, Paul C Gordon, Paul Der Mesropian, Paul Galiwango, Paul Hauptman, Paul Kennedy, Paula Beardsley, Paula García-González, Paulo Cury Rezende, Paulo Ricardo Caramori, Pavel S Kozlov, Pedro Canas Silva, Pedro Gabriel Melo Barros E Silva, Pedro Píccaro de Oliveira, Pedro Carvalho, Pedro Modas, Pedro Rio, Peeyush Jain, Peiyu He, Peter A McCullough, Peter H Stone, Peter M Pollak, Peter Douglass, Peter Henriksen, Peter OKane, Peter Ong, Philip Jones, Philip Rogal, Philippe Généreux, Philippe Menasche, Philippe Rheault, Phoebe Goold, Pierre Gervais, Pierre Michaud, Pilar Calvillo, Ping Chai, Piotr Jakubowski, Piotr Pruszczyk, Piotr Slomka, Piyamitr Sritara, Poay-Huan Loh, Poonam Sonawane, Pouneh Samadi, Pragnesh P Parikh, Prakash Deedwania, Pranav M Patel, Praneeth Polamuri, Pratiksha Sharma, Precilia Vasquez, Preeti Kamath, Prince Thomas, Priyadarshani Arambam, Puja K Mehta, Purvez Grant, Pushpa Naik, Qi Zhong, Qian Zhao, Qiang Zhou, Qianqian Yuan, Qin Yu, Qingxian Li, Qiulan Xie, Qiutang Zeng, R J Vindhya, R James Gerlach, Rachel King, Rada Vučić, Radmila Lyubarova, Radoslaw Pracon, Raewyn Fisher, Rafael Beyar, Rafael Diaz, Rafael Selgas, Raffaele Bugiardini, Raffaele Fanelli, Raisa Kavalakkat, V S Rajalekshmi, Rajat S Barua, Rajeev Menon, Rajesh Gopalan Nair, Rajesh Francis, Rajiv Narang, Rakesh Yadav, Ralph Alan Huston, T Ramakrishnan, Ramesh de Silva, Rami El Mahmoud, Ramiro Carvalho, Ramon de Jesús-Pérez, Ramona Stevens, Ran Leng, Ranjan Kachru, Ranjit Kumar Nath, Raquel Sanchez, Raven R Dwyer, Raven Lee, Ray Wyman, Raymond C Wong, Raymond W Little, Raymundo Ocaranza Sanchez, Rebecca J Wimmer, Rebecca Bariciano, Rebecca Otis, Rebekah R Herrmann, Reem Yunis, Reinette Hampson, Renato Abdala Karam, Renee C Hessian, Renee Kaneshiro, Reshma Ravindran, Reto Andreas Gamma, Reyna Bhandari, Reza Arsanjani, Ricardo L Lopes, Ricardo Mendes Oliveira, Ricardo Costa, Richa Bhatt, Richard F Davies, Richard H J Trimlett, Richard Goldweit, Rik Hermanides, Rine Nakanishi, Rinu R Sidh, Risha Patel, Rita Coram, Rizwan A Siddiqui, Rob S Beanlands, Robert J Hamburger, Robert K Riezebos, Robert M Donnino, Robert Bojar, Robert Chilton, Robert Guyton, Robert Henderson, Robert Kornberg, Robert Leber, Robert Mao, Robert Stenberg, Roberta P Santos, Roberto René Favaloro, Roberto Amati, Rodolfo G S D Lima, Rodrigo J Cerci, Rogerio Tumelero, Rohit Tandon, Roma Tewari, Romalisa Miranda-Peats, Ron Wald, Ronald A Mastouri, Ronald G Morford, Ronald G Schwartz, Ronald P Pedalino, Rongrong Hu, Ronnell A Hansen, Ronny A Cohen, Rory Hachamovitch, Rosa Homem, Rosa Sandonato, Rosane Laimer, Rosann Gans, Roxanne Yost, Roy Mathew, Rubén Baleón-Espinosa, Ruben Ramos, Rubine Gevorgyan, Rui Ferreira, Rui Jing, Ruth Pérez-Fernández, S K Dwivedi, S Ramakrishnan, Saadat Khan, Sabahat Bokhari, Sabu Thomas, Sadath Lubna, Sajeeda Parveen Khan, Sajeev Chakanalil Govindan, Saket Girotra, Saleem Kassam, Sallie Canada, Salvador Cruz-Flores, Samaa Mohamed, Samantha Ly, Sameh El Kaffas, Samia Massalha, Sampoornima Setty, Samuel Nwosu, Sandeep Seth, Sandeep Singh, Sander R Niehe, Sandra M Rivest, Sandra S Zier, Sandra Ahoud, Sandy Carr, Sanjay Ganapathi, Sanjay Shetty, Sanjeev Sharma, Santa Jimenez, Santhosh Satheesh, Santiago A Garcia, Sara Fernandez, Sara Karlsson, Sara Salkind, Sara Temiyasathit, Sarah Medina Rodriguez, Sarah Beaudry, Sarah Hadjih, Sarah Williams, Sarah Zahrani, Sarju Ralhan, Sasa Hinic, Sasko Kedev, Satinder Singh, Satoshi Yasuda, Satvic Cholenahally Manjunath, Sau Lee, Scott M Kaczkowski, Scott Kinlay, Sean W Hayes, Sebastian Sobczak, Senait Asier, Sergey A Sayganov, Seth I Sokol, Shaheen Pandie, Shaiful Azmi Yahaya, Shamir Mehta, Shao-Ping Nie, Sharad Chandra, Sharder Islam, Sharon Tai, Sheetal Rupesh Karwa, Sheri Ussery, Sheromani Bajaj, Sherron C Crook, Shigeyuki Nishimura, Shintaro Nakano, Shirin Heydari, Shiv Kumar Choudhary, Shivali Patel, Shobana Ganesan, Shruti Pandey, Shuyang Zhang, Shweta Hande, Siddharth Gadage, Sik-Yin V Tan, Silvia Zottis Poletti, Silvia Riera, Silvia Valbuena, Simon Walsh, Simona Maspoli, Simone Savaris, Si-Ting Feng, So Yang Cho, Solomon Yakubov, Songlin Zhu, Songtao Wang, Sonia Guerrero, Sonika Gupta, Sonja Salinger Martinovic, Sonya Brons, Sorin Brener, Sothinathan Gurunathan, Souheil Saba, Soundarya Nayak, Sowjanya Reddy, Srinivasa Potluri, Sriram Sudarshan, Srun Kuanprasert, Stacie Van Oosterhout, Stamatios Lerakis, Stanley E Cobos, Stefan C Bertog, Stefan M Simović, Stefan Weikl, Stefano Di Marco, Stefano Provasoli, Stephanie A Tirado, Stephanie C Boer, Stephanie M Lane, Stephanie Ferket, Stephanie Kelly, Stephanie Wasmiller, Stephen H McKellar, Stephen P Hoole, Stephen Fremes, Stephen Preston, Steve Leung, Steven A Fein, Steven J Lindsay, Steven P Sedlis, Steven Giovannone, Steven Michael, Steven Weitz, Stijn van Vugt, Subhash Banerjee, Sudhir Naik, Suellen Hosino, Sukie Desire, Sukit Yamwong, Suku T Thambar, Sulagna Mookherjee, Suman Singh, Sundeep Mishra, Sunil Kumar Verma, Supap Kulthawong, Supatchara Khwakhong, Surendra Naik, Suresh Babu, Surin Woragidpoonpol, Suryaprakash Narayanappa, Susan Derbyshire, Susan Gent, Susan Mathus, Susan Milbrandt, Susan Moore, Susan Regan, Susan Stinson, Susan Webber, Susana Silva, Susanna Stevens, Susanne Gruensfelder, Suthara Aramcharoen, Suvarna Kolhe, Suzana Tavares, Suzanne Arnold, Suzanne Welsh, Svetlana Apostolovic, Swapna Kunhunny, Ta-Chuan Hung, Taissa Zappernick, Tali Sharir, Talita Silva, Tamara Colaiácovo Soares, Tapan Umesh Pillay, Tarun K Mittal, Tatiana Trifonova, Tauane Bello Duarte, Tauqir Huk, Téodora Dutoiu, Terrance Chua, Terry Weyand, Thabitha Charles, Theodoros Kofidis, Theresa McCreary, Thierry Lefevre, Thippeekaa Arumairajah, Thitipong Tepsuwan, Thomas J Mulhearn, Thomas M Meyer, Thomas P Rocco, Thomas R Downes, Thomas Crain, Thomas Haldis, Thomas Mathew, Thomas Redick, Thounaojam Indira Devi, Thuraia Nageh, Tia Cauthren, Tiago Silva, Tiffany Little, Tijana Andric, Tina Harding, Titus Lau, Tiziana Formisano, Tiziano Moccetti, Tomasz Ciurus, Tomasz Mazurek, Tomasz Tarchalski, Toshiyuki Nagai, Tri Tran, Tricia Youn, Trish Tucker, Trudie Milner, Tuhina Bose, Tushar Kotecha, Udo Sechtem, Uma S Valeti, Umberto Cucchini, Umesh Badami, Upendra Kaul, V K Bahl, V S Narain, Valentina Casali, Valeria Godoy, Valerie Robesyn, Vamshi P Priya, Vandana Yadav, Vera McKinney, Veronica De Lenges, Veronica Tinnirello, Vicente Miro, Victor Navarro, Victoria Gumerova, Victoria Hernandez, Vidya Seeratan, Vijay Kumar, Vikentiy Y Kozulin, Viktoria Bulkley, Vilmar Veiga Jr, Vincent Setang, C P Vineeth, Virginai Pubull Nuñez, Virginia Fernández-Figares, Vitor Gomes, Viviana Gabriel, Viviane Dos Santos, Viviane Almeida, Vlad A Iliescu, Vladan Mudrenovic, Vladimir Dzavik, Vojislav L Giga, Walter Enrique Mogrovejo, Wan Xian Chan, Wanda C Marfori, Wanda Parker, Warangkana Mekara, Wassim Nona, Wayne Old, Wayne Pennachi, Weerachai Nawarawong, Wei Chen, Wei Su, Weibing Xing, Wei-Ren Lan, Wenda Crawford, Wendy L Stewart, Wendy Drewes, Wenhua Lin, William B Abernethy, William D Salerno, William F Fearon, William Vergoni, William Weintraub, Winnie C Sia, Wlodzimierz J Musial, Xacobe Flores-Ríos, Xavier Garcia-Moll Marimon, Xi Su, Xiang Ma, Xiangqiong Gu, Xiao Wang, Xiaomei Li, Xiaowei Yao, Xin Fu, Xin Su, Xin Zeng, Xinchun Yang, Xiuhong Li, Xuehua Fang, Xutong Wang, Yaming Geng, Yan Yan, Yanek Pépin-Dubois, Yanfu Wang, Yang Wang, Yanmeng Tian, Yaping Huang, Yechen Han, Yesenia Zambrano, Yi-Hsuan Yang, Ying Tung Sia, Yining Yang, Yitong Ma, Yolayfi Peralta, Yongjian Wu, Yu Kunwu, Yu Zhao, Yudong Peng, Yueh-Hung Lin, Yulan Zhao, Yumei Dong, Yunhai Zhao, Yutthaphan Wannasopha, Yvonne Taul, Zakir Sahul, Zalina Kudzoeva, Zbigniew Kalarus, Zeljko Z Markovic, Zhen Huang, Zheng Ji, Zhenyu Liu, Zhou Yue, Zhulin Zhang, Zhuxi Li, Zile Singh Meharwal, Ziliang Bai, Zixiang Yu, Zohra Huda, Zoltan Davidovits
Subjects: Male, Cardiac Catheterization, Computed Tomography Angiography, medicine.medical_treatment, Myocardial Ischemia, Coronary Disease, Coronary Artery Disease, Kaplan-Meier Estimate, 030204 cardiovascular system & hematology, Coronary Angiography, ISCHEMIA Research Group, law.invention, Angina, Coronary artery disease, 0302 clinical medicine, Randomized controlled trial, law, Cardiovascular Disease, Myocardial Revascularization, 030212 general & internal medicine, Coronary Artery Bypass, 11 Medical and Health Sciences, Cardiac catheterization, General Medicine, Middle Aged, humanities, Cardiovascular Diseases, Cardiology, Female, Human, medicine.medical_specialty, Ischemia, Article, 03 medical and health sciences, Geriatric cardiology, Percutaneous Coronary Intervention, General & Internal Medicine, Internal medicine, medicine, Humans, Angina, Unstable, Aged, business.industry, Coronary Artery Bypa, Percutaneous coronary intervention, Bayes Theorem, medicine.disease, Heart failure, Quality of Life, business
Abstract: BACKGROUND: Among patients with stable coronary disease and moderate or severe ischemia, whether clinical outcomes are better in those who receive an invasive intervention plus medical therapy than in those who receive medical therapy alone is uncertain. METHODS: We randomly assigned 5179 patients with moderate or severe ischemia to an initial invasive strategy (angiography and revascularization when feasible) and medical therapy or to an initial conservative strategy of medical therapy alone and angiography if medical therapy failed. The primary outcome was a composite of death from cardiovascular causes, myocardial infarction, or hospitalization for unstable angina, heart failure, or resuscitated cardiac arrest. A key secondary outcome was death from cardiovascular causes or myocardial infarction. RESULTS: Over a median of 3.2 years, 318 primary outcome events occurred in the invasive-strategy group and 352 occurred in the conservative-strategy group. At 6 months, the cumulative event rate was 5.3% in the invasive-strategy group and 3.4% in the conservative-strategy group (difference, 1.9 percentage points; 95% confidence interval [CI], 0.8 to 3.0); at 5 years, the cumulative event rate was 16.4% and 18.2%, respectively (difference, -1.8 percentage points; 95% CI, -4.7 to 1.0). Results were similar with respect to the key secondary outcome. The incidence of the primary outcome was sensitive to the definition of myocardial infarction; a secondary analysis yielded more procedural myocardial infarctions of uncertain clinical importance. There were 145 deaths in the invasive-strategy group and 144 deaths in the conservative-strategy group (hazard ratio, 1.05; 95% CI, 0.83 to 1.32). CONCLUSIONS: Among patients with stable coronary disease and moderate or severe ischemia, we did not find evidence that an initial invasive strategy, as compared with an initial conservative strategy, reduced the risk of ischemic cardiovascular events or death from any cause over a median of 3.2 years. The trial findings were sensitive to the definition of myocardial infarction that was used. (Funded by the National Heart, Lung, and Blood Institute and others; ISCHEMIA ClinicalTrials.gov number, NCT01471522.).
Published: 2020

33. Changes in IL-27 and its effect on CD4 + T cells in patients with coronary artery disease

Author: Yifan Cai, Hongxia Tang, Wenjuan Tang, Wenbin Xu, Yue Wang, Yan Ding, Jian Yu, Chengliang Pan, Zhiyang Li, Yudong Peng, Ruirui Zhu, Kunwu Yu, Qiutang Zeng, and Yucheng Zhong
Abstract: Objective：Coronary artery disease (CAD) is an immune-mediated chronic disease, and interleukin-27(IL-27) regulates CD4+ T cell differentiation. However, little is known about its effects on CAD. Therefore, we aimed to investigate the changes of IL-27 and its effect on CD4+ T cells in patients with CAD.Methods: The severity of coronary artery stenosis was assessed by Gensini score, and the concentrations of plasma IL-27, ox-LDL were measured by ELISA. qRT-PCR and Western Blotting (WB) were performed to evaluate the mRNA and protein expression of T-bet, IFN-γ, GATA-3, and RORγt. After monocytes were stimulated with recombinant IL-2 and/or IL-27, CD4+IFN-γ+T cells, CD4+IL-4+T cells, CD4+IL-17+T cells, CD4+LAP+T cells and CD4+CD25+Foxp3+ Tregs were counted by flow cytometry. Results: Plasma IL-27 levels were significantly elevated in patients with Acute Coronary Syndromes (ACS). IL-27 levels were positively correlated with ox-LDL and Gensini scores (P < 0.01) and ox-LDL levels were positively correlated with Gensini scores (P < 0.01). The more severe the stenosis in CAD patients, the more Th1 and Th17 cells, and the less Th2, CD4+CD25+Foxp3+Tregs and CD4+LAP+T cells. IL-27 can increase the expression of T-bet and IFN-γ, and inhibit the expression of RORγt and GATA-3, and finally promote the differentiation of CD4+T cells into Th1 cells, and inhibit the differentiation of Th2, Th17, CD4+CD25+Foxp3+Tregs and CD4+LAP+T cells.Conclusion: IL-27 regulates CAD by increasing the expression of T-bet and IFN-γ and inhibiting the expression of RORγt and GATA-3, thereby increasing the frequency of Th1 cells and decreasing the frequency of Th2, Th17, CD4+CD25+Foxp3+Tregs and CD4+LAP+T cells.
Published: 2022

34. Ablation of CXCR4 expression in cardiomyocytes exacerbates isoproterenol-induced cell death and heart failure

Author: min cheng, Can Chen, kunwu Yu, Qiutang Zeng, and Feng Zhu
Abstract: Heart failure is an ageing-associated disease. CXCR4, a seven-transmembrane-spanning Gi-coupled receptor for the SDF-1 chemokine, plays a critical role in organogenesis, healthy ageing, vascular post-injury repair and regeneration; however, the specific role of cardiomyocyte CXCR4 in heart function and the pathogenesis of heart failure is incompletely understood. We hypothesize that CXCR4 expression in cardiomyocytes is protective during β-adrenoceptor/Gs stress-induced cardiac dysfunction. Cardiomyocyte-specific CXCR4 knockout (CXCR4-CMKO) mice were generated by crossing CXCR4fl/fl and MHC-Cre+/− mice and shown to display normal cardiac structure and function in the basal state until at least 4 months old. However, following continuous administration of isoproterenol (Iso) via an osmotic mini-pump, their ventricular myocardial contractility, dilation, cardiomyocyte apoptosis, and interstitial fibrosis were worsened compared to that of control MHC-Cre+/− littermates under same treatment. In the cultured H9C2 cardiomyocytes, SDF-1 treatment markedly attenuated Iso-induced apoptosis and reduction in phospho-Akt, and these protective effects were diminished by knockdown of CXCR4 or by co-treatment with Gi inhibitors. Thus, cardiomyocyte SDF-1/CXCR4 signaling alleviates β-adrenergic stress-induced cell death and cardiac adverse remodeling, thus may be harnessed for treatment of heart failure.
Published: 2022

35. Phosphorylcholine-Primed Dendritic Cells Aggravate the Development of Atherosclerosis in ApoE−/− Mice

Author: Yue Wang, Qingwei Ji, Wen-Bing Xu, Yan Ding, Chengliang Pan, Kunwu Yu, Qiutang Zeng, Qian Dong, Yudong Peng, Kai Meng, Yucheng Zhong, Yu-Zhen Wei, Zhengfeng Zhu, Jian Yu, Haitao Sun, and Ruirui Zhu
Subjects: CD86, Cellular immunity, Innate immune system, CD40, biology, Chemistry, Phosphorylcholine, hemic and immune systems, chemical and pharmacologic phenomena, Inflammation, General Medicine, Immune system, Antigen, Immunology, medicine, biology.protein, medicine.symptom
Abstract: Background: Atherosclerosis is an inflammatory disease involving activation of adaptive and innate immune responses to antigens, including oxidized low-density lipoprotein (oxLDL) and phosphorylcholine (PC). Dendritic cells (DCs), which are antigen-presenting cells that activate T cells, are present in atherosclerotic lesions and are activated in immune organs. However, the mechanism by which PC promotes atherosclerosis is unclear. Methods and Results: To evaluate whether PC promotes atherosclerosis via DCs, 2×105 DCs activated by PC-keyhole limpet hemocyanin (DCs+PC-KLH) were injected into ApoE-/- mice and the features of the plaques and the effects of the DCs on cellular and humoral immunity against PC-KLH were determined. Mice injected with DCs+PC-KLH had significantly larger atherosclerotic lesions than controls, with increased inflammation in the lesions and plaque instability. Furthermore, DCs+PC-KLH were characterized using flow cytometry after coculture of bone marrow-derived DCs and naive T cells. DCs+PC-KLH showed an inflammatory phenotype, with increased CD86, CD40, and major histocompatibility complex Class II molecules (MHC-II), which promoted PC-specific T helper (Th) 1 and Th17 cell differentiation in vivo and in vitro. Moreover, 2 weeks after the administration of DCs+PC-KLH to mice, these mice produced PC- and oxLDL-specific IgG2a, compared with no production in the controls. Conclusions: These findings suggest that DCs presenting PC promote specific immunity to PC, increase lesion inflammation, and accelerate atherosclerosis, which may explain how PC promotes atherosclerosis.
Published: 2021

36. IL-37 Expression in Patients with Abdominal Aortic Aneurysm and Its Role in the Necroptosis of Vascular Smooth Muscle Cells

Author: Yan Ding, Yue Wang, Yifan Cai, Chengliang Pan, Chao Yang, Miao Wang, Xiaoyu Qi, Jing Ye, Qingwei Ji, Jian Yu, Wenbin Xu, Kunwu Yu, and Qiutang Zeng
Subjects: Aging, Article Subject, Interleukin-6, Tumor Necrosis Factor-alpha, Angiotensin II, Myocytes, Smooth Muscle, Endothelial Cells, Cell Biology, General Medicine, Biochemistry, Muscle, Smooth, Vascular, Necroptosis, cardiovascular system, Humans, Aortic Aneurysm, Abdominal, Interleukin-1
Abstract: Background. Our previous studies have shown that interleukin- (IL-) 37 plays a protective role in patients and animal models with coronary artery disease. However, the role of IL-37 in patients with abdominal aortic aneurysm (AAA), another artery disease, is yet to be elucidated. Methods and Results. AAA tissues and plasma samples were obtained from patients with or without surgical intervention. Normal renal aortic tissues were collected from kidney transplant donors. Our findings established that in AAA, IL-37 was distributed in endothelial cells, macrophages, and vascular smooth muscle cells (VSMCs) and that it was chiefly concentrated in VSMCs. Furthermore, the expression was found to be downregulated compared with that in normal artery tissues. Immunofluorescence showed that, unlike normal arteries, IL-37 was translocated to the nucleus of VSMCs in AAA. Moreover, in patients with AAA, the expressions of IL-37, IL-6, and tumor necrosis factor- (TNF-) α were increased in the plasma in comparison with the healthy controls. Correlation analysis revealed that IL-37 was positively correlated with IL-6, TNF-α, age, aneurysm diameter, and blood pressure. Furthermore, human aortic vascular smooth muscle cells (HASMCs) were stimulated with angiotensin II (AngII) in vitro to simulate smooth muscle cell (SMC) damage in AAA. A decrease in IL-37 expression and an increase in receptor-interacting serine/threonine-protein kinase 3 (RIPK3) expression were observed in HASMCs stimulated with AngII. On this basis, inhibition of RIPK3 with GSK’872 significantly attenuated necroptosis. Moreover, the necroptosis rates were significantly lowered in HASMCs treated with recombinant IL-37, whereas the rates were enhanced when the cells were depleted of the interleukin. Immunoblotting results showed that both exogenous and endogenous IL-37 could affect the expressions of RIPK3, NLRP3, and IL-1β. Also, the phosphorylation of RIPK3 and p65 was affected. Meanwhile, IL-37 promoted the transition of SMC from proliferative type to contractile type. Conclusions. The expression of IL-37 in VSMCs decreases in patients with AAA, whereas IL-37 supplementation suppresses RIPK3-mediated necroptosis and promotes the transition of VSMCs from proliferative to contractile type.
Published: 2021

37. GARP and GARP-Treated tDC Prevented the Formation of Atherosclerotic Plaques in ApoE−/- Mice

Author: Yucheng Zhong, Yuzhou Liu, Chengliang Pan, Ruirui Zhu, Qiutang Zeng, Wenbin Xu, Yifan Cai, Yudong Peng, Xiaobo Mao, Jian Yu, Lun Huang, Kunwu Yu, Peng Cheng, Yan Ding, Yi Mao, and Yue Wang
Subjects: medicine.medical_specialty, Apoe mice, GARP-tDC, Chemistry, Immunology, FOXP3, Biological activity, Treg cell, Phenotype, In vitro, Endocrinology, GARP, Internal medicine, Foxp3, LAP, medicine, Immunology and Allergy, Secretion, IL-2 receptor, atherosclerosis, Journal of Inflammation Research, Original Research
Abstract: Yifan Cai,1 Qiutang Zeng,1 Yuzhou Liu,2 Ruirui Zhu,1 Kunwu Yu,1 Wenbin Xu,1 Yue Wang,1 Yan Ding,1 Jian Yu,1 Chengliang Pan,1 Yudong Peng,1 Yi Mao,1 Peng Cheng,1 Lun Huang,1 Xiaobo Mao,1 Yucheng Zhong1 1Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, Peopleâs Republic of China; 2Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, Peopleâs Republic of ChinaCorrespondence: Yucheng ZhongLaboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jie-Fang Avenue, Wuhan, 430022, Peopleâs Republic of ChinaTel +86-27-85726423Fax +86-27-85726425Email zyc811029@126.comPurpose: This study aims to clarify the specific mechanism by which GARP affects the atherosclerotic plaques in ApoEâ/- mice and the effect of GARP-tDC on atherosclerosis.Methods: The mice were randomly divided into three groups: the control group, the GARP-overexpressed group and the GARP-inhibited group. After 12 weeks, all the mice were euthanized, and the specimens were collected. In vitro, experiments were conducted to observe the effect of GARP on DC phenotype and the changes of the proportion of CD4+CD25+Foxp3+ Treg cells when GARP-tDCs were co-cultured with CD4+ T cells. Furthermore, adoptive transmission of GARP-tDCs was used to observe the effect on atherosclerotic plaque in mice.Results: The GARP-overexpressed group enhanced the biological activity of Foxp3+ CD4+CD25+ Tregs and resulted in increased expression of LAP in T cells. In addition, the GARP-overexpressed group significantly suppressed the function of Th1 and Th17, and decreased the secretion of INF-Î³ and IL-17A. Thus, GARP had a protective effect on atherosclerosis. In vitro, we found that GARP-tDC had a tolerance-inducing phenotype, and GARP-tDC also had the ability to induce tolerance when co-cultured with CD4+ T cells. More importantly, adoptive transmission of GARP-tDCs reduced the size of atherosclerotic plaques.Conclusion: GARP and the GARP-tDC play protective roles in atherosclerosis. The protective effect of GARP on atherosclerosis is achieved by increasing CD4+CD25+Foxp3+ Treg cells and inhibiting the production of IFN-Î³ and IL-17A.Keywords: GARP, Foxp3, GARP-tDC, atherosclerosis, LAP
Published: 2021

38. Interleukin‐38 alleviates cardiac remodelling after myocardial infarction

Author: Qiutang Zeng, Yuzhen Wei, Kunwu Yu, Yin Lan, Ruirui Zhu, Yan Ding, Yue Wang, Yucheng Zhong, Wenbin Xu, and Haitao Sun
Subjects: Male, 0301 basic medicine, Cardiac function curve, medicine.medical_specialty, medicine.medical_treatment, Myocardial Infarction, Apoptosis, Inflammation, T-Lymphocytes, Regulatory, 03 medical and health sciences, 0302 clinical medicine, interleukin‐38, Internal medicine, Troponin I, Immune Tolerance, medicine, Animals, Myocytes, Cardiac, RNA, Messenger, Myocardial infarction, Ventricular Remodeling, business.industry, cardiac remodelling, Interleukin, Dendritic Cells, Original Articles, Cell Biology, Acquired immune system, medicine.disease, Fibrosis, Survival Analysis, Mice, Inbred C57BL, Phenotype, 030104 developmental biology, Cytokine, 030220 oncology & carcinogenesis, Cardiology, Molecular Medicine, Original Article, Myocardial fibrosis, medicine.symptom, business, Interleukin-1
Abstract: Excessive immune‐mediated inflammatory reaction plays a deleterious role in ventricular remodelling after myocardial infarction (MI). Interleukin (IL)‐38 is a newly characterized cytokine of the IL‐1 family and has been reported to exert a protective effect in some autoimmune diseases. However, its role in cardiac remodelling post‐MI remains unknown. In this study, we found that the expression of IL‐38 was increased in infarcted heart after MI induced in C57BL/6 mice by permanent ligation of the left anterior descending artery. In addition, our data showed that ventricular remodelling after MI was significantly ameliorated after recombinant IL‐38 injection in mice. This amelioration was demonstrated by better cardiac function, restricted inflammatory response, attenuated myocardial injury and decreased myocardial fibrosis. Our results in vitro revealed that IL‐38 affects the phenotype of dendritic cells (DCs) and IL‐38 plus troponin I (TNI)‐treated tolerogenic DCs dampened adaptive immune response when co‐cultured with CD4+T cells. In conclusion, IL‐38 plays a protective effect in ventricular remodelling post‐MI, one possibility by influencing DCs to attenuate inflammatory response. Therefore, targeting IL‐38 may hold a new therapeutic potential in treating MI.
Published: 2019

39. Corrigendum: Galectin-9: A Suppressor of Atherosclerosis?

Author: Yan Ding, Yucheng Zhong, Qiutang Zeng, Jian Yu, Kunwu Yu, Yue Wang, and Ruirui Zhu
Subjects: lcsh:Immunologic diseases. Allergy, T Cell Immunoglobulin Mucin-3, Chemistry, Immunology, Correction, Arteriosclerosis, medicine.disease, regulatory T cells, law.invention, T helper cells, T-cell immunoglobulin mucin 3, law, Cancer research, medicine, Immunology and Allergy, Suppressor, atherosclerosis, lcsh:RC581-607, Galectin-9, Galectin
Published: 2021

40. Role of IL-37- and IL-37-Treated Dendritic Cells in Acute Coronary Syndrome

Author: Qiutang Zeng, Kunwu Yu, Chengliang Pan, Yucheng Zhong, Fangyuan Zhang, and Ruirui Zhu
Subjects: Aging, Chemokine, Acute coronary syndrome, Inflammation, Review Article, Biochemistry, Proinflammatory cytokine, Mice, Immunity, Medicine, Animals, Humans, Secretion, Acute Coronary Syndrome, biology, QH573-671, business.industry, Cell Biology, General Medicine, Dendritic Cells, Acquired immune system, medicine.disease, Immunology, biology.protein, medicine.symptom, business, Cytology, Reperfusion injury, Interleukin-1
Abstract: As a chronic inflammatory disease, atherosclerosis is a leading cause of morbidity and mortality in most countries. Inflammation is responsible for plaque instability and the subsequent onset of acute coronary syndrome (ACS), which is one of the leading causes of hospitalization. Therefore, exploring the potential mechanism underlying ACS is of considerable concern, and searching for alternative therapeutic targets is very urgent. Interleukin-37 (IL-37) inhibits the production of proinflammatory chemokines and cytokines and acts as a natural inhibitor of innate and adaptive immunity. Interestingly, our previous study with murine models showed that IL-37 alleviated cardiac remodeling and myocardial ischemia/reperfusion injury. Of note, our clinical study revealed that IL-37 is elevated and plays a beneficial role in patients with ACS. Moreover, dendritic cells (DCs) orchestrate both immunity and tolerance, and tolerogenic DCs (tDCs) are characterized by more secretion of immunosuppressive cytokines. As expected, IL-37-treated DCs are tolerogenic. Hence, we speculate that IL-37- or IL-37-treated DCs is a novel therapeutic possibility for ACS, and the precise mechanism of IL-37 requires further study.
Published: 2021

41. Clinical Characteristics and Prognosis of 244 Cardiovascular Patients Suffering From Coronavirus Disease in Wuhan, China

Author: Qiutang Zeng, Meian He, Xiang Wang, Tangchun Wu, Caiying Hu, Liang Leng, Bende Liu, Longxian Cheng, Ruirui Zhu, Kai Huang, Mulatibieke Keerman, Hongquan Guan, Qingwei Ji, Zihan Ke, Kai Meng, and Yudong Peng
Subjects: Male, Epidemiology, Comorbidity, 030204 cardiovascular system & hematology, SARS‐CoV‐2, 0302 clinical medicine, cardiovascular disease, 030212 general & internal medicine, Original Research, Aged, 80 and over, biology, Mortality rate, Middle Aged, Prognosis, Survival Rate, C-Reactive Protein, coronavirus disease, Cardiovascular Diseases, Female, Coronavirus Infections, Cardiology and Cardiovascular Medicine, Procalcitonin, severe acute respiratory syndrome coronavirus 2, Adult, China, medicine.medical_specialty, Pneumonia, Viral, Betacoronavirus, 03 medical and health sciences, COVID‐19, Internal medicine, medicine, Humans, Pandemics, Survival rate, Aged, Retrospective Studies, SARS-CoV-2, business.industry, C-reactive protein, respiratory failure, COVID-19, Fibrinogen, Retrospective cohort study, medicine.disease, Respiratory failure, Heart failure, biology.protein, Tomography, X-Ray Computed, business, Body mass index, Biomarkers, Follow-Up Studies
Abstract: Background The coronavirus disease 2019 (COVID‐19) has developed into a global outbreak. Patients with cardiovascular disease (CVD) with COVID‐19 have different clinical characteristics and prognostic outcomes. This study aimed to summarize the clinical characteristics and laboratory indicators of patients with COVID‐19 with CVD, especially the critically ill patients. Methods and Results This study included 244 patients diagnosed with COVID‐19 and CVD (hypertension, coronary heart disease, or heart failure). The patients were categorized into critical (n=36) and noncritical (n=208) groups according to the interim guidance of China’s National Health Commission. Clinical, laboratory, and outcome data were collected from the patients’ medical records and compared between the 2 groups. The average body mass index of patients was significantly higher in the critical group than in the noncritical group. Neutrophil/lymphocyte ratio, and C‐reactive protein, procalcitonin, and fibrinogen, and d ‐dimer levels at admission were significantly increased in the critical group. The all‐cause mortality rate among cases of COVID‐19 combined with CVD was 19.26%; the proportion of coronary heart disease and heart failure was significantly higher in deceased patients than in recovered patients. High body mass index, previous history of coronary heart disease, lactic acid accumulation, and a decrease in the partial pressure of oxygen were associated with death. Conclusions All‐cause mortality in patients with COVID‐19 with CVD in hospitals is high. The high neutrophil/lymphocyte ratio may be a predictor of critical patients. Overweight/obesity combined with coronary heart disease, severe hypoxia, and lactic acid accumulation resulting from respiratory failure are related to poor outcomes. Registration URL: https://www.chictr.org.cn ; Unique identifier: ChiCTR2000029865.
Published: 2020

42. The Long Noncoding RNA Hotair Regulates Oxidative Stress and Cardiac Myocyte Apoptosis during Ischemia-Reperfusion Injury

Author: Wenbin Xu, Jian Yu, Kunwu Yu, Jiao Jiao, Yucheng Zhong, Ruirui Zhu, Zhengfeng Zhu, Yudong Peng, Boyuan Wang, Kai Meng, Qiutang Zeng, Yan Ding, and Xiaobo Mao
Subjects: 0301 basic medicine, Male, Aging, Article Subject, Apoptosis, Myocardial Reperfusion Injury, 030204 cardiovascular system & hematology, medicine.disease_cause, Biochemistry, 03 medical and health sciences, Mice, 0302 clinical medicine, medicine, Myocyte, Animals, Myocytes, Cardiac, Protein kinase A, Gene knockdown, QH573-671, Chemistry, Cardiac myocyte, HOTAIR, Cell Biology, General Medicine, medicine.disease, Oxidative Stress, 030104 developmental biology, Cancer research, RNA, Long Noncoding, Cytology, Reperfusion injury, Oxidative stress, Research Article
Abstract: Oxidative stress and subsequent cardiac myocyte apoptosis play central roles in the initiation and progression of myocardial ischemia-reperfusion (I/R) injury. Homeobox transcript antisense intergenic RNA (Hotair) was previously implicated in various heart diseases, yet its role in myocardial I/R injury has not been clearly demonstrated. Mice with cardiac-restricted knockdown or overexpression of Hotair were exposed to I/R surgery. H9c2 cells were cultured and subjected to hypoxia/reoxygenation (H/R) stimulation to further verify the role and underlying mechanisms of Hotair in vitro. Histological examination, molecular detection, and functional parameters were determined in vivo and in vitro. In response to I/R or H/R treatment, Hotair expression was increased in a bromodomain-containing protein 4-dependent manner. Cardiac-restricted knockdown of Hotair exacerbated, whereas Hotair overexpression prevented I/R-induced oxidative stress, cardiac myocyte apoptosis, and cardiac dysfunction. Mechanistically, we observed that Hotair exerted its beneficial effects via activating AMP-activated protein kinase alpha (AMPKα). Further detection revealed that Hotair activated AMPKα through regulating the enhancer of zeste homolog 2/microRNA-451/calcium-binding protein 39 (EZH2/miR-451/Cab39) axis. We provide the evidence that endogenous lncRNA Hotair is an essential negative regulator for oxidative stress and cardiac myocyte apoptosis in myocardial I/R injury, which is dependent on AMPKα activation via the EZH2/miR-451/Cab39 axis.
Published: 2020

43. Down-regulation and Clinical Implication of Galectin-9 Levels in Patients with Acute Coronary Syndrome and Chronic Kidney Disease

Author: Li Zhao, Ruirui Zhu, Jian-Hua Xie, Qiutang Zeng, and Yucheng Zhong
Subjects: Adult, Male, medicine.medical_specialty, Acute coronary syndrome, Galectins, Renal function, Down-Regulation, Type 2 diabetes, Comorbidity, Biochemistry, Impaired glucose tolerance, chemistry.chemical_compound, Internal medicine, Genetics, medicine, Humans, Acute Coronary Syndrome, Receptors, Immunologic, Renal Insufficiency, Chronic, Blood urea nitrogen, Hepatitis A Virus Cellular Receptor 2, Aged, Creatinine, business.industry, Forkhead Transcription Factors, Middle Aged, medicine.disease, Endocrinology, chemistry, Female, business, Kidney disease, Lipoprotein, Glomerular Filtration Rate
Abstract: In various autoimmune diseases, Galecin-9 (Gal-9) has been shown to regulate the T-cell balance by decreasing Th1 and Th17, while increasing the number of regulatory T cells (Tregs). However, the role of Gal-9 in the patients with acute coronary syndrome (ACS) and chronic kidney disease (CKD) remains unclear. This study aims to measure the Gal-9 levels in serum and peripheral blood mononuclear cells (PBMCs) in patients with ACS plus CKD and examine their clinical implication. The serum levels of Gal-9 were determined by enzyme-linked immunosorbent assay (ELISA), the expression levels of Gal-9, Tim-3, and Foxp3 mRNA in PBMCs were detected by real-time reverse transcription-polymerase chain reaction (RT-PCR), and the expression of Gal-9 on the surface of PBMCs and in PBMCs was analyzed by flow cytometry. Furthermore, the correlation of serum Gal-9 levels with anthropometric and biochemical variables in patients with ACS plus CKD was analyzed. The lowest levels of Gal-9 in serum and PBMCs were found in the only ACS group, followed by the ACS+CKD group, and the normal coronary artery (NCA) group, respectively. Serum Gal-9 levels were increased along with the progression of glomerular filtration rate (GFR) categories of G1 to G4. Additionally, serum Gal-9 levels were negatively correlated with high-sensitivity C-reactive protein (hs-CRP), estimated GFR (eGFR), and lipoprotein(a), but positively with creatinine, age, osmotic pressure, and blood urea nitrogen (BUN). Notably, serum Gal-9 was independently associated with hs-CRP, osmotic pressure, and lipoprotein(a). Furthermore, serum Gal-9 levels were elevated in patients with type 2 diabetes (T2DM) and impaired glucose tolerance (IGT) in ACS group. It was suggested that the levels of Gal-9 in serum and PBMCs were decreased in patients with simple ACS and those with ACS plus CKD, and hs-CRP, eGFR, osmotic pressure and T2DM may have an influence on serum Gal-9 levels.
Published: 2020

44. The protective effect of L-carnitine on ischemia-reperfusion heart

Author: Jiang, Xie, Qiutang, Zeng, and Le, Wang
Published: 2006
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45. The cardioprotective effect of thymoquinone on ischemia‐reperfusion injury in isolated rat heart via regulation of apoptosis and autophagy

Author: Junhui Xiao, Yan Shi, Qiutang Zeng, Zhe Cao, and Zun-Ping Ke
Subjects: Male, 0301 basic medicine, Cardiac function curve, Cardiotonic Agents, Cardiac marker, Myocardial Infarction, Apoptosis, Myocardial Reperfusion Injury, 030204 cardiovascular system & hematology, Pharmacology, Biochemistry, Superoxide dismutase, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Heart Rate, Lactate dehydrogenase, Autophagy, Benzoquinones, Ventricular Pressure, medicine, Animals, Creatine Kinase, MB Form, Plant Oils, Rats, Wistar, Molecular Biology, Thymoquinone, Analysis of Variance, L-Lactate Dehydrogenase, biology, Heart, Isolated Heart Preparation, Cell Biology, Malondialdehyde, medicine.disease, Rats, Oxidative Stress, 030104 developmental biology, chemistry, biology.protein, Reperfusion injury
Abstract: Thymoquinone (TQ), as the active constituents of black cumin (Nigella sativa) seed oil, has been reported to have potential protective effects on the cardiovascular system. This study aimed to investigate the effects and the underlying mechanisms of TQ on myocardial ischemia-reperfusion (I/R) injury in Langendorff-perfused rat hearts. Wister rat hearts were subjected to I/R and the experimental group were pretreated with TQ prior to I/R. Hemodynamic parameters, myocardial infarct size, cardiac marker enzymes, superoxide dismutase (SOD), malondialdehyde (MDA) content, and cardiomyocyte apoptosis were assayed. Compared with the untreated group, TQ preconditioning significantly improved cardiac function, reduced infarct size, decreased cardiac lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) levels, suppressed enedoxidative stress, and apoptosis. In addition, TQ treatment promoted autophagy, which was partially reversed by chloroquine (CQ), a kind of autophagy blocker. Our study suggests that TQ can protect heart against I/R injury, which is associated with anti-oxidative and anti-apoptotic effects through activation of autophagy.
Published: 2018

46. Astragalus prevents diabetic rats from developing cardiomyopathy by downregulating angiotensin II type2 receptors expression

Author: Changyun, Li, Linsheng, Cao, and Qiutang, Zeng
Published: 2004
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47. Inhibition of microRNA-155 ameliorates cardiac fibrosis in the process of angiotensin II-induced cardiac remodeling

Author: Wenhan Ma, Xiaofei Yan, Fen Hu, ZhaoHui Wang, Qiutang Zeng, Ya Wang, Yuzhen Wei, Lianhua Yan, and Shuai Lu
Subjects: Male, 0301 basic medicine, Cardiac function curve, Cancer Research, Cardiac fibrosis, Heart Ventricles, microRNA-155, cardiac fibrosis, 030204 cardiovascular system & hematology, Biology, Pharmacology, Biochemistry, Transforming Growth Factor beta1, Mice, 03 medical and health sciences, Suppressor of Cytokine Signaling 1 Protein, 0302 clinical medicine, Fibrosis, Genetics, medicine, Animals, Smad3 Protein, Ventricular remodeling, Molecular Biology, Cells, Cultured, Pressure overload, Ventricular Remodeling, Angiotensin II, Myocardium, Antagomirs, Heart, Articles, Fibroblasts, medicine.disease, Mice, Inbred C57BL, MicroRNAs, suppressor of cytokine signaling 1, 030104 developmental biology, Oncology, Leukocytes, Mononuclear, cardiovascular system, Cancer research, Molecular Medicine, Myocardial fibrosis, cardiac remodeling, Myofibroblast, Spleen
Abstract: Cardiac fibrosis triggered by pressure overload represents one of the major challenges in the treatment of cardiovascular diseases. MicroRNA (miRNA/miR)‑155, a member of the small RNA family, has previously been demonstrated to be associated with cardiac inflammation. However, the effect of miR‑155 on cardiac fibrosis induced by angiotensin II (Ang II), particularly in cardiac fibroblasts, requires further investigation. The present study aimed to investigate the effect of miR‑155 in Ang II‑induced cardiac fibrosis using animal models and cardiac fibroblasts. Animal models were established in male miR‑155‑/‑ and wild‑type (WT) C57Bl/6J mice (10‑12 weeks old) by Ang II infusion using subcutaneously implanted minipumps. After 8 weeks of Ang II infusion, the results demonstrated that the deletion of miR‑155 in mice markedly ameliorated ventricular remodeling compared with WT mice, as demonstrated by restricted inflammatory responses, decreased heart size, improved cardiac function and reduced myocardial fibrosis. In vitro, overexpression of miR‑155 in cardiac fibroblasts led to significantly increased fibroblast to myofibroblast transformation. However, this effect was abrogated by miR‑155 silencing. In conclusion, the results of the present study indicate that genetic loss of miR‑155 in mice ameliorates cardiac fibrotic remodeling following pressure overload. Therefore, inhibiting miR‑155 may have potential as an adjunct to reduce cardiac inflammation in the treatment of cardiac fibrosis.
Published: 2017

48. Cardioprotective Effects of Malvidin Against Isoproterenol-Induced Myocardial Infarction in Rats: A Mechanistic Study

Author: Yudong Peng, Lili Jiang, Hui Li, Qiutang Zeng, Hui Wei, Longxian Cheng, and Shu-Ping Wan
Subjects: Male, medicine.medical_specialty, Antioxidant, Heart Diseases, medicine.medical_treatment, Phytochemicals, Myocardial Infarction, Enzyme-Linked Immunosorbent Assay, 030204 cardiovascular system & hematology, Pharmacology, Antioxidants, Superoxide dismutase, Lipid peroxidation, Anthocyanins, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Internal medicine, Lactate dehydrogenase, medicine, Animals, Rats, Wistar, chemistry.chemical_classification, Glutathione Peroxidase, biology, Chemistry, Plant Extracts, Superoxide Dismutase, Glutathione peroxidase, Animal Study, Myocardium, Isoproterenol, Heart, General Medicine, Glutathione, Catalase, Malvidin, Rats, 030220 oncology & carcinogenesis, biology.protein, Cardiology, Creatine kinase, Lipid Peroxidation, Phytotherapy
Abstract: BACKGROUND Malvidin (alvidin-3-glucoside) is a polyphenol that belongs to the class of natural anthocyanin, which is abundantly found in red wines, colored fruits, and the skin of red grapes. Therefore, the current investigation was intended to evaluate the effect of malvidin against myocardial infarction induced by isoproterenol in the rats. MATERIAL AND METHODS The cardioprotective effects was assessed by determining the effect of malvidin on the activities of endogenous antioxidants - catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH) - and on the levels of lipid peroxidation and serum marker enzymes. The serum levels of IL-6 and TNF-α were also determined using an enzyme-linked immunosorbent assay (ELISA) kit. RESULTS The present study demonstrated a significant cardioprotective effect of malvidin by restoring the defensive activities of endogenous antioxidants - catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH) - and by reducing the levels of lipid peroxidation and serum marker enzymes lactate dehydrogenase (LD) and creatine kinase (CK). Malvidin significantly ameliorated the histopathological changes and impaired mitochondria in the cardiac necrosis stimulated with isoproterenol. Additionally, the results also demonstrated that nuclear translocation of Nrf-2 and subsequent HO-1 expression might be associated with nuclear factor kappa B (NF-κB) pathway activation. CONCLUSIONS Our findings suggest that malvidin exerts cardioprotective effects that might be due to possible strong antioxidant and anti-inflammatory activities. Therefore, this study provides the basis for the development of malvidin as a safe and effective treatment of myocardial infarction.
Published: 2017

49. CD4+ CD25+ GARP+ regulatory T cells display a compromised suppressive function in patients with dilated cardiomyopathy

Author: Quan Luo, Xin Su, Kunwu Yu, Wenbin Xu, Hui Wei, Yucheng Zhong, Huairui Shi, Qiutang Zeng, Ruirui Zhu, Junhui Xiao, Yuzhen Wei, and Haitao Sun
Subjects: 0301 basic medicine, chemistry.chemical_classification, Heart disease, Immunology, FOXP3, Interleukin, hemic and immune systems, chemical and pharmacologic phenomena, Dilated cardiomyopathy, 030204 cardiovascular system & hematology, Biology, medicine.disease, Phenotype, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Immune system, chemistry, Interferon, medicine, Immunology and Allergy, cardiovascular diseases, Glycoprotein, medicine.drug
Abstract: Dilated cardiomyopathy (DCM) is a lethal inflammatory heart disease and closely connected with dysfunction of the immune system. Glycoprotein A repetitions predominant (GARP) expressed on activated CD4+ T cells with suppressive activity has been established. This study aimed to investigate the frequency and function of circulating CD4+ CD25+ GARP+ regulatory T (Treg) cells in DCM. Forty-five DCM patients and 46 controls were enrolled in this study. There was a significant increase in peripheral T helper type 1 (Th1) and Th17 number and their related cytokines [interferon-γ (IFN-γ), interleukin (IL-17)], and an obvious decrease in Treg number, transforming growth factor-β1 (TGF-β1 ) levels and the expression of forkhead box P3 (FOXP3) and GARP in patients with DCM compared with controls. In addition, the suppressive function of CD4+ CD25+ GARP+ Treg cells was impaired in DCM patients upon T-cell receptor stimulation detected using CFSE dye. Lower level of TGF-β1 and higher levels of IFN-γ and IL-17 detected using ELISA were found in supernatants of the cultured CD4+ CD25+ GARP+ Treg cells in DCM patients compared with controls. Together, our results indicate that CD4+ CD25+ GARP+ Treg cells are defective in DCM patients and GARP seems to be a better molecular definition of the regulatory phenotype. Therefore, it might be an attractive stategy to pay more attention to GARP in DCM patients.
Published: 2017

50. The IL-2/Anti-IL-2 Complex Attenuates Cardiac Ischaemia-Reperfusion Injury Through Expansion of Regulatory T Cells

Author: Ming Li, Junhui Xiao, Chuanyin Xiong, Yuzhen Wei, Kunwu Yu, and Qiutang Zeng
Subjects: Male, 0301 basic medicine, Physiology, Apoptosis, Antigen-Antibody Complex, 030204 cardiovascular system & hematology, Pharmacology, T-Lymphocytes, Regulatory, lcsh:Physiology, Mice, 0302 clinical medicine, Medicine, lcsh:QD415-436, Myocytes, Cardiac, lcsh:QP1-981, Antibodies, Monoclonal, Interleukin-10, medicine.anatomical_structure, Cytokines, Immunotherapy, medicine.symptom, Ischaemia/reperfusion injury, Myocardial Reperfusion Injury, Spleen, Inflammation, Proinflammatory cytokine, lcsh:Biochemistry, Transforming Growth Factor beta1, 03 medical and health sciences, In vivo, Splenocyte, Animals, Regulatory T-lymphocytes (Tregs), business.industry, Myocardium, Hemodynamics, Interleukin-2 Receptor alpha Subunit, Th1 Cells, medicine.disease, Mice, Inbred C57BL, Disease Models, Animal, 030104 developmental biology, Interleukin-2, Th17 Cells, Myocardial fibrosis, business, Reperfusion injury
Abstract: Background/Aims: Regulatory T cells (Tregs) can suppress immunologic damage in myocardial ischaemia/reperfusion injury (MIRI), however, the isolation and ex vivo expansion of these cells for clinical application remains challenging. Here, we investigated whether the IL-2/anti-IL-2 complex (IL-2C), a mediator of Treg expansion, can attenuate MIRI in mice. Methods: Myocardial I/R was surgically induced in male C57BL/6 mice, aged 8-10 weeks, that were randomly assigned to 1) sham group (Sham), 2) Phosphate Buffered Saline (PBS), 3) IL-2-anti-IL-2 Ab complex (IL-2C), or 4) sham group, 5) PBS, 6) IL-2C after MIRI, or 7) IL-2C, 8) IL-2C+anti-CD25 mAbs, or 9) IL-2C; 10) IL-2C+anti-TGF-β1 mAbs, 11) IL-2C+anti-IL-10 mAbs. The following parameters were measured at different time points: infarct area, myocardial apoptosis, splenocytes, the inhibitory function of Tregs, and presence of inflammatory factors. In addition, immunohistochemistry analysis was performed. Results: We observed that Tregs were activated in response to MIRI. IL-2C administered before MIRI induced Treg expansion in both spleen and heart, attenuated Th1 and Th17 cell numbers, improved myocardial function, and attenuated both infiltration of inflammatory cells and apoptosis after MIRI. Furthermore, IL-2C administration reduced expression of inflammatory cytokines in the heart and attenuated proliferation of splenic cells. Depletion of Tregs with anti-CD25 mAb abrogated the beneficial effects of IL-2C. However, IL-2C–mediated myocardial protection was not dependent on either IL-10 or TGF-β. In addition, IL-2C administration after MIRI did not reduce infarct area, but did improve myocardial function slightly and reduced myocardial fibrosis. Conclusion: Our results demonstrate that IL-2C–induced Treg expansion attenuates MIRI and improves myocardial recovery in vivo, suggesting that IL-2C is a promising therapeutic target for myocardial IRI.
Published: 2017

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