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2. IRF-1 mediates the suppressive effects of mTOR inhibition on arterial endothelium

Author

Peng, Kai, Fan, Xing, Li, Qiannan, Wang, Yiying, Chen, Xiaolin, Xiao, Pingxi, Passerini, Anthony G, Simon, Scott I, and Sun, ChongXiu

Subjects
Biomedical and Clinical Sciences, Medical Physiology, Cardiovascular Medicine and Haematology, Animals, Apoptosis, Cell Cycle Checkpoints, Cell Proliferation, Cells, Cultured, Endothelial Cells, Endothelium, Vascular, Femoral Artery, Humans, Interferon Regulatory Factor-1, Mice, Mice, Knockout, Naphthyridines, Signal Transduction, Sirolimus, TOR Serine-Threonine Kinases, Transfection, Endothelium, Cell proliferation, Transcription factor, Drug-eluting stents, mTOR, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Biochemistry and cell biology, Cardiovascular medicine and haematology, Medical physiology
Abstract

AimsMammalian target of rapamycin (mTOR) inhibitors used in drug-eluting stents (DES) to control restenosis have been found to delay endothelialization and increase incidence of late-stent thrombosis through mechanisms not completely understood. We revealed that mTOR inhibition (mTORi) upregulated the expression of cell growth suppressor IRF-1 in primary human arterial endothelial cells (HAEC). This study aimed to examine how mTOR-regulated IRF-1 expression contributes to the suppressive effect of mTORi on arterial endothelial proliferation.Methods and resultsWestern blotting, quantitative PCR, and a dual-luciferase reporter assay indicated that mTOR inhibitors rapamycin and torin 1 upregulated IRF-1 expression and increased its transcriptional activity. IRF-1 in turn contributed to the suppressive effect of mTORi by mediating HAEC apoptosis and cell cycle arrest in part through upregulation of caspase 1 and downregulation of cyclin D3, as revealed by CCK-8 assay, Annexin V binding assay, measurement of activated caspase 3, BrdU incorporation assay, and matrigel tube formation assay. In a mouse model of femoral artery wire injury, administration of rapamycin inhibited EC recovery, an effect alleviated by EC deficiency of IRF-1. Chromatin immunoprecipitation assay with HAEC and rescue expression of wild type or dominant-negative IRF-1 in EC isolated from Irf1-/- mice confirmed transcriptional regulation of IRF-1 on the expression of CASP1 and CCND3. Furthermore, mTORi activated multiple PKC members, among which PKCζ was responsible for the growth-inhibitory effect on HAEC. Activated PKCζ increased IRF1 transcription through JAK/STAT-1 and NF-κB signaling. Finally, overexpression of wild type or mutant raptor incapable of binding mTOR indicated that mTOR-free raptor contributed to PKCζ activation in mTOR-inhibited HAEC.ConclusionsThe study reveals an IRF-1-mediated mechanism that contributes to the suppressive effects of mTORi on HAEC proliferation. Further study may facilitate the development of effective strategies to reduce the side effects of DES used in coronary interventions.

Published
2020

7. Improved Risk Prediction of Acute Myocardial Infarction in Patients With Stable Coronary Artery Disease Using an Amino Acid‐Assisted Model.

Author

Zhao, Yi-Jing, Li, Yong, Wang, Feng-Xiang, Lv, Hao, Qu, Yaoyao, Qi, Lian-Wen, Xiao, Pingxi, and Jiang-Shan, Tan

Subjects
LIQUID chromatography-mass spectrometry, MYOCARDIAL infarction, CORONARY artery disease, RECEIVER operating characteristic curves, AMINO acids
Abstract

Patients with stable coronary artery disease (CAD) are at an increased risk of acute myocardial infarction (AMI), particularly among older individuals. Developing a reliable model to predict AMI occurrence in these patients holds the potential to expedite early diagnosis and intervention. This study is aimed at establishing a circulating amino acid‐assisted model, incorporating amino acid profiles alongside clinical variables, to predict AMI risk. A cohort of 874 CAD patients from two independent centers was analyzed. Plasma amino acid levels were quantified using liquid chromatography tandem mass spectrometry (LC‐MS/MS) employing a targeted metabolomics approach. This methodology incorporated 13C isotope‐labeled internal standards for precise quantification of 27 amino acids. Univariate logistic regression was applied to identify differentially expressed amino acids that distinguished between stable CAD and AMI patients. To assess prediction performance, receiver operating characteristic (ROC) curve and nomogram analyses were utilized. Five amino acids—lysine, methionine, tryptophan, tyrosine, and N6‐trimethyllysine—emerged as potential biomarkers (p < 0.05), exhibiting significant differences in their expression levels across the two centers when comparing stable CAD with AMI patients. For AMI risk prediction, the base model, utilizing 12 clinical variables, achieved areas under the curve (AUC) of 0.7387 in the discovery phase (n = 623) and 0.8205 in the external validation set (n = 251). Notably, the integration of these five amino acids into the prediction model significantly enhanced its performance, increasing the AUC to 0.7651 in the discovery phase (Delong's test, p = 1.43e‐02) and to 0.8958 in the validation set (Delong's test, p = 8.91e‐03). In conclusion, the circulating amino acid‐assisted model effectively enhances the prediction of AMI risk among CAD patients, indicating its potential clinical utility in facilitating early detection and intervention. [ABSTRACT FROM AUTHOR]

Published
2024
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25. 2023 Chinese expert consensus on the impact of COVID-19 on the management of cardiovascular diseases

Author

Bai, Feng, Pu, Jun, Che, Wenliang, Chen, Jiyan, Chen, Mao, Chen, Wei, Chen, Xiaoping, Chen, Yundai, Cheng, Xianwu, Cheng, Xiang, Cong, Hongliang, Dai, Cuilian, Fan, Dali, Fu, Guosheng, Gao, Lei, Gao, Chuanyu, Gao, Wei, Ge, Junbo, He, Ben, Hu, Tao, Huang, Congxin, Huang, Jing, Huo, Yong, Jia, Shaobin, Jiang, Jun, Jing, Zhicheng, Kong, Xiangqing, Li, Lang, Li, Yan, Li, Yigang, Li, Zhijuan, Liang, Chun, Lin, Xianhe, Liu, Xianxia, Liu, Xuebo, Lu, Chengzhi, Ma, Genshan, Ma, Yitong, Mao, Wei, Mei, Xia, Ning, Zhongping, Ou, Jiafu, Slaj, Shaderdin, Shen, Chengxing, Shi, Haiming, Shi, Hong, Shi, Bei, Su, Xi, Sun, Ningling, Tang, Qizhu, Wang, Fang, Wang, Changqian, Wang, Jin, Wu, Yanqing, Wu, Yongjian, Xia, Yunlong, Xiang, Dingcheng, Xiao, Pingxi, Xie, Ping, Xiong, Dingding, Xu, Yawei, Yang, Jiefu, Yang, Lixia, Yu, Zaixin, Yuan, Zuyi, Yuan, Haitao, Zhang, Guogang, Zhang, Heng, Zhang, Jian, Zhang, Li, Zhang, Ruiyan, Zhang, Shuning, Zhang, Shuyang, Zhang, Zheng, Zhao, Guoan, Zhao, Xianxian, Zheng, Jingang, Zheng, Haoyi, Zhou, Daxin, Zhou, Shenghua, and Zhou, Yujie

Abstract

The primary site of infection in COVID-19 exhibit is the respiratory system, but multiple organ systems could be affected. The virus could directly invade cardiomyocytes. Alternatively, cytokine storm could lead to myocardial injury. More importantly, the management of existing cardiovascular diseases must be re-examined in COVID-19 due to, for example, interaction between antiviral agents and with a wide variety of pharmacological agents. The Branch of Cardiovascular Physicians of Chinese Medical Doctor Association organized a panel of experts in cardiovascular and related fields to discuss this important issue, and formulated the “2023 Chinese Expert Consensus on the Impact of COVID-19 on the Management of Cardiovascular Diseases.” The Consensus was drafted on the basis of systematic review of existing evidence and diagnosis and treatment experience, and covers three major aspects: myocardial injury caused by COVID-10 and COVID-19 vaccine, the impact of COVID-19 on patients with cardiovascular disease, and the impact of COVID-19 on the cardiovascular system of healthy people, and rehabilitation guidance recommendations. The Consensus involves 11 core clinical issues, including incidence, pathogenesis, clinical manifestations, treatment strategies, prognosis, and rehabilitation. It is our hope that this Consensus will provide a practical guidance to cardiologists in the management of cardiovascular diseases in the new era of COVID-19 pandemic.

Published
2023
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26. Neuraminidase 1 is a driver of experimental cardiac hypertrophy

Author

Chen, Qian-Qian, primary, Ma, Gaoxiang, additional, Liu, Jin-Feng, additional, Cai, Yuan-Yuan, additional, Zhang, Jun-Yuan, additional, Wei, Ting-Ting, additional, Pan, An, additional, Jiang, Shujun, additional, Xiao, Yibei, additional, Xiao, Pingxi, additional, Song, Jiangping, additional, Li, Ping, additional, Zhang, Lei, additional, and Qi, Lian-Wen, additional

Published
2021
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29. Imperatorin’s Effect on Myocardial Infarction Based on Network Pharmacology and Molecular Docking

Author

Zhang, Ruizhe, Wang, Peng, Jin, Yao, Xie, Qingya, Xiao, Pingxi, and Mehata, Abhishesh

Abstract

Purpose:Myocardial infarction (MI), a severe cardiovascular disease, is the result of insufficient blood supply to the myocardium. Despite the improvements of conventional therapies, new approaches are needed to improve the outcome post‐MI. Imperatorin is a natural compound with multiple pharmacological properties and potential cardioprotective effects. Therefore, this work investigated imperatorin’s therapeutic effects and its mechanism of action in an MI mouse model. Methods: Network pharmacology, molecular docking, and experimental validation were performed for exploring the pharmacokinetic properties, therapeutic effects, and molecular targets of imperatorin in MI. Permanent ligation of the left anterior descending artery was performed in male C57BL/6 mice to induce MI before treatment with imperatorin once per day for 1 week. Echocardiography, heart histology, RNA sequencing, and quantitative reverse transcriptase polymerase chain reaction (qRT‐PCR) as well as western blotting were carried out for evaluating cardiac function and structure, as well as gene and protein expression. Results: Imperatorin significantly improved cardiac function, preserved cardiac structure, attenuated cardiac remodeling and fibrosis, and reduced cardiomyocyte apoptosis in MI mice. Eight differentially expressed genes overlapping with key target genes were found, two upregulated and six downregulated. A key target in signaling pathways associated with imperatorin effect in MI was angiotensin‐converting enzyme (ACE). Imperatorin inhibited ACE–angiotensin II (Ang II)–angiotensin II Type 1 receptor (AT1R) axis in MI mice. Conclusion: Imperatorin attenuated MI by inhibiting the ACE–Ang II–AT1R axis. Thus, imperatorin might be considered a potential therapeutic agent to cure MI.

Published
2025
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36. Bmi1 and BRG1 drive myocardial repair by regulating cardiac stem cell function in acute rheumatic heart disease

Author

Min Xu, Liu Niannian, Kai Zhang, Bangshun Ge, Tao Zhiwen, Lu Xinzheng, and Xiao Pingxi

Subjects
0301 basic medicine, Cancer Research, Pathology, medicine.medical_specialty, Heart disease, Cell, Inflammation, General Medicine, Articles, Biology, Cell cycle, medicine.disease, Molecular medicine, 03 medical and health sciences, 030104 developmental biology, medicine.anatomical_structure, Immunology and Microbiology (miscellaneous), BMI1, Immunology, medicine, Rheumatic fever, medicine.symptom, Stem cell
Abstract

Rheumatic heart disease (RHD) occurs due to the accumulation of complications associated with rheumatic fever, and it results in high morbidity and mortality. The majority of cases of RHD are diagnosed in the chronic stages, when treatment options are limited. A small reservoir of cardiac stem cells is responsible for maintaining cardiac homeostasis and repairing tissue damage. Understanding the role of cardiac stem cells and the various proteins responsible for their functions in different pathological stages of RHD is an important area of investigation. Polycomb complex protein BMI-1 (Bmi1) and transcription activator BRG1 (BRG1) are associated with the maintenance of stemness in various types of stem cells. The present study investigated the role served by Bmi1 and BRG1 in cardiac stem cells during various pathological stages of RHD through immunohistochemistry and western blotting. A rat model of RHD was established via immunization with the Group A Streptococcus M5 protein. The rat was demonstrated to develop acute RHD 2 months after the final immunization, characterized by cardiac inflammation and tissue damage. Chronic RHD was identified 4 months after the final immunization, revealed by cardiac tissue compression and shrinkage. Expression of the cardiac stem cell marker mast/stem cell growth factor receptor kit was identified to be elevated during acute RHD, but downregulated in the chronic stages of RHD. A similar pattern of expression was revealed for Bmi1 and BRG1, indicating that they serve a role in regulating cardiac stem cell proliferation during acute RHD. These results suggest that cardiac stem cells serve a supportive role in the acute, but not chronic, stages of RHD via expression of Bmi1 and BRG1.

Published
2017

40. Lipid profile perturbations in the plasma and lungs of mice with LPS-induced acute lung injury revealed by UHPLC-ESI-Q Exactive HF MS analysis.

Author

Shan, Jinjun, Qian, Wenjuan, Kang, An, Peng, Linxiu, Xie, Tong, Lin, Lili, Di, Liuqing, Xiao, Pingxi, and Zhou, Wei

Subjects
*BLOOD lipids, *BLOOD plasma, *LUNG injuries, *LIPOPOLYSACCHARIDES, *INFLAMMATION, *LIPID metabolism, *HIGH performance liquid chromatography, *TANDEM mass spectrometry
Abstract

Highlights • UHPLC-ESI-Q Exactive HF MS-based lipidomics was applied to profile various lipids. • About 77 and 13 differential lipids were successfully profiled. • The lipidomics reveled the correlation between inflammation and lipid metabolism. Abstract An UHPLC-ESI-Q Exactive HF MS-based lipidomics method was successfully applied to profile various lipids from the plasma and lungs of mice intranasally challenged with lipopolysaccaride (LPS). Response trends of lipids to LPS were graphically represented by variable importance in projection (VIP) plot, heat map, and bar plot. As a result, 77 differential lipids in the lung and 13 differential lipids in the plasma were identified by comparison between healthy and LPS- induced mice. These results revealed the correlation between inflammation and lipids metabolism. The differentially regulated lipids could also be potentially used as biomarkers for inflammation. [ABSTRACT FROM AUTHOR]

Published
2019
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