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4 results on '"Rixin Xiong"'

1. Vaspin Alleviates Sepsis-Induced Cardiac Injury and Cardiac Inflammation by Inhibiting Kallikrein 7 in Mice

Author

Na Yin, Fuze Pan, Lingyue Qiu, Zicong Yang, Rixin Xiong, Lei Shi, Ying Shi, Ning Wu, Kui Wu, Qingkuan Li, Daojun Wen, Qili Huang, Yuyan Zhang, Yuhong Mi, and Qingwei Ji

Subjects
Pathology, RB1-214
Abstract

Background. Vaspin is an important adipokine that is involved in cardiovascular diseases. This study is aimed at investigating whether vaspin participates in sepsis-induced cardiac injury and explored the possible mechanism. Methods. First, cecal ligation and puncture (CLP) and lipopolysaccharide (LPS) were used to establish a mouse model of sepsis, and cardiac vaspin expression was examined. In addition, after pretreatment with vaspin or phosphate-buffered saline (PBS), wild-type (WT) mice underwent CLP to establish a septic model and received sham as a control. Finally, WT mice and kallikrein 7 (KLK7-/-) mice were underwent CLP with or without vaspin pretreatment. Results. Mice that underwent CLP and were administered LPS exhibited increased vaspin expression in both the heart and serum compared with sham- or saline-treated mice. In CLP mice, pretreatment with vaspin reduced mortality and alleviated the expression of cardiac injury markers and cardiac dysfunction. In addition, vaspin reduced the cardiac levels of CD45+ cells and CD68+ cells, alleviated the cardiac inflammatory response, and reduced cardiomyocyte apoptosis. The protective effects of vaspin on CLP mice were masked by the deletion of KLK7, which was demonstrated to be a downstream signal of vaspin. Conclusions. Vaspin alleviates cardiac inflammation and plays a protective role in sepsis-induced cardiac injury by reducing KLK7 expression.

Published
2022
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2. ADAMTS-5 Decreases in Aortas and Plasma From Aortic Dissection Patients and Alleviates Angiotensin II-Induced Smooth Muscle-Cell Apoptosis

Author

Tao Zeng, Jianting Gan, Yu Liu, Lei Shi, Zhengde Lu, Yan Xue, Rixin Xiong, Ling Liu, Zicong Yang, Yingzhong Lin, and Jun Yuan

Subjects
acute aortic dissection, ADAMTS-5, extracellular matrix, smooth muscle cells, matrix metalloproteinase, apoptosis, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Background: Acute aortic dissection (AAD) is associated with degeneration of the aortic media and accompanied by vascular extracellular matrix (ECM) remodeling. Recently, a disintegrin and metalloproteinase with thrombospondin type 1 motifs-5 (ADAMTS-5) has been reported to be involved in ECM remodeling and vascular diseases. The aim of this study was to examine ADAMTS-5 levels in AAD patients and investigate the underlying mechanisms.Methods: Aortic tissue samples were collected from normal donors and AAD patients, and the expression of ADAMTS-5 was analyzed in all aortic tissues. In addition, plasma levels of ADAMTS-5, matrix metalloproteinase (MMP)-2 and MMP-9, and tumor necrosis factor-α (TNF-α) were measured in repeated samples from AAD patients and compared to the non-AAD (NAD) group. In addition, we investigated the effects of ADAMTS-5 in smooth muscle cell (SMC) apoptosis.Results: The results showed that ADAMTS-5 expression was significantly reduced in the aortas of AAD patients and that SMCs were the main source of ADAMTS-5. In addition, the plasma ADAMTS-5 level was lower, but plasma MMP-2, MMP-9, and TNF-α levels were increased in the AAD patients. Multivariate linear regression analyses showed that a decreased ADAMTS-5 level in patients was independently associated with an increased risk of AAD. Furthermore, recombinant human ADAMTS-5 significantly ameliorated angiotensin (Ang II)-evoked SMC apoptosis.Conclusions: ADAMTS-5 shows promise as a novel potential biomarker for AAD, and regulation of SMC is a possible mechanism for the effects of ADAMTS-5.

Published
2020
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3. ADAMTS-5 Decreases in Aortas and Plasma From Aortic Dissection Patients and Alleviates Angiotensin II-Induced Smooth Muscle-Cell Apoptosis

Author

Jianting Gan, Zhengde Lu, Lei Shi, Yu Liu, Tao Zeng, Yan Xue, Yingzhong Lin, Rixin Xiong, Ling Liu, Zicong Yang, and Jun Yuan

Subjects
0301 basic medicine, lcsh:Diseases of the circulatory (Cardiovascular) system, medicine.medical_specialty, matrix metalloproteinase, extracellular matrix, Cardiovascular Medicine, 030204 cardiovascular system & hematology, Matrix metalloproteinase, Extracellular matrix, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Renin–angiotensin system, medicine, Original Research, Aortic dissection, Thrombospondin, Metalloproteinase, acute aortic dissection, business.industry, ADAMTS, apoptosis, ADAMTS-5, medicine.disease, Angiotensin II, smooth muscle cells, 030104 developmental biology, Endocrinology, lcsh:RC666-701, Cardiology and Cardiovascular Medicine, business
Abstract

Background: Acute aortic dissection (AAD) is associated with degeneration of the aortic media and accompanied by vascular extracellular matrix (ECM) remodeling. Recently, a disintegrin and metalloproteinase with thrombospondin type 1 motifs-5 (ADAMTS-5) has been reported to be involved in ECM remodeling and vascular diseases. The aim of this study was to examine ADAMTS-5 levels in AAD patients and investigate the underlying mechanisms. Methods: Aortic tissue samples were collected from normal donors and AAD patients, and the expression of ADAMTS-5 was analyzed in all aortic tissues. In addition, plasma levels of ADAMTS-5, matrix metalloproteinase (MMP)-2 and MMP-9, and tumor necrosis factor-α (TNF-α) were measured in repeated samples from AAD patients and compared to the non-AAD (NAD) group. In addition, we investigated the effects of ADAMTS-5 in smooth muscle cell (SMC) apoptosis. Results: The results showed that ADAMTS-5 expression was significantly reduced in the aortas of AAD patients and that SMCs were the main source of ADAMTS-5. In addition, the plasma ADAMTS-5 level was lower, but plasma MMP-2, MMP-9, and TNF-α levels were increased in the AAD patients. Multivariate linear regression analyses showed that a decreased ADAMTS-5 level in patients was independently associated with an increased risk of AAD. Furthermore, recombinant human ADAMTS-5 significantly ameliorated angiotensin (Ang II)-evoked SMC apoptosis. Conclusions: ADAMTS-5 shows promise as a novel potential biomarker for AAD, and regulation of SMC is a possible mechanism for the effects of ADAMTS-5.

Published
2020
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4. Thrombospondin 1 Is Increased in the Aorta and Plasma of Patients With Acute Aortic Dissection

Author

Zicong Yang, Lei Shi, Ling Liu, Yan Xue, Tao Zeng, Yu Liu, Yingzhong Lin, Jianting Gan, Jun Yuan, Rixin Xiong, Min Huang, and Zhengde Lu

Subjects
Adult, Male, endocrine system, medicine.medical_specialty, Blotting, Western, Enzyme-Linked Immunosorbent Assay, 030204 cardiovascular system & hematology, Matrix metalloproteinase, Polymerase Chain Reaction, Muscle, Smooth, Vascular, Thrombospondin 1, 03 medical and health sciences, Aortic aneurysm, 0302 clinical medicine, immune system diseases, medicine.artery, Internal medicine, Renin–angiotensin system, medicine, Animals, Humans, 030212 general & internal medicine, Aorta, Abdominal, Cells, Cultured, Aorta, biology, business.industry, virus diseases, Interleukin, Middle Aged, medicine.disease, Nitric oxide synthase, Mice, Inbred C57BL, Aortic Dissection, Endocrinology, Gene Expression Regulation, Apoptosis, Acute Disease, cardiovascular system, biology.protein, RNA, Female, Cardiology and Cardiovascular Medicine, business, Aortic Aneurysm, Abdominal
Abstract

Background Previous studies have shown that thrombospondin 1 (TSP-1) is involved in cardiovascular diseases, such as atherosclerosis and abdominal aortic aneurysm. However, TSP-1 expression levels in human aortic dissection (AD) remain unknown. Methods TSP-1 levels were detected in aortas collected from control subjects and AD patients. The TSP-1, interleukin (IL) 6, matrix metalloproteinase (MMP) 2, and MMP9 levels in plasma from non-AD patients and AD patients were measured. In addition, the effects of recombinant mouse TSP-1 protein on macrophage differentiation and smooth muscle cell (SMC) apoptosis were investigated. Results Compared with the aortas from control subjects, aortas from AD patients showed a significant increase in TSP-1 expression, especially in the torn sections. SMCs and endothelial cells produced TSP-1, but SMCs were the main source. TSP-1, IL-6, MMP2, and MMP9 levels were higher in AD patients than in non-AD patients, and plasma IL-6, MMP2, and MMP9 levels were positively correlated with TSP-1 levels in AD patients. Simple linear regression analysis and multivariate linear regression analysis showed that TSP-1 levels were independently correlated with the onset of AD. In cultured cells, recombinant mouse TSP-1 further increased inducible nitric oxide synthase (iNOS) mRNA expression in angiotensin (Ang) II-treated macrophages, whereas it reduced B-cell lymphoma-2 (Bcl2) mRNA levels and increased Bcl2-associated X protein (Bax) mRNA levels in Ang II-treated SMCs. Conclusions TSP-1 level is significantly increased in AD patients and might participate in AD via promoting classically activated macrophage (M1) macrophage differentiation and SMC apoptosis.

Published
2018

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