Cardiac stem cells improve the electrophysiological stability and ventricular fibrillation threshold via ANGII/AT1R/TGF-beta1/SMAD/CX43 signaling pathway

doi:10.3969/j.issn.2095-4344.2016.28.018

Abstract

Abstract:

BACKGROUND: Previous studies have demonstrated that the electrophysiological stability and ventricular fibrillation threshold after myocardial infarction in rats are significantly improved in the mid-term of cardiac stem cell transplantation, but relative regulatory mechanism and pathway remain unclear.
OBJECTIVE: To explore the relative molecular regulatory mechanism of cardiac stem cells improving the electrophysiological stability and ventricular fibrillation threshold after myocardial infarction in rats.
METHODS: Myocardial infarction was induced in 20 Sprague-Dawley rats by ligation of the left anterior descending coronary, which were then randomized into two groups (n=10 per group) and were subjected to the injection of cardiac stem cells labeled with PKH26 in phosphate buffer solution (cardiac stem cell group) or the same amount of phosphate buffer solution (PBS) alone (PBS group) into the local infarct zone at 2 weeks after modeling, respectively. Six weeks later, relevant signaling molecules involved in the ANGII/AT1R/TGF-β1/SMAD/Cx43 pathway were all examined in myocardial tissues of the left ventricle and harvested blood samples.
RESULTS AND CONCLUSION: Compared with the PBS group, expressions of connexin 43 in different zones of the left ventricle were significantly increased in the cardiac stem cell group (P < 0.01); there was a significant reduction of the angiotensin II level in plasma and different regions of the left ventricular (P < 0.05; P < 0.01). Furthermore, in the cardiac stem cell group, expressions of angiotensin II type I receptor, transforming growth factor-β1, SMAD2 and SMAD3 were significantly decreased (P < 0.01). Whereas SMAD7 was significantly elevated (P < 0.05) in different areas of the left ventricle compared with the phosphate buffer solution group. These findings suggest that the cardiac stem cell transplantation can improve the electrophysiological stability and ventricular fibrillation threshold after myocardial infarction by enhancing the expression of connexin 43 via ANGII/AT1R/TGF-beta1/SMAD/CX43 signaling pathway.

中国组织工程研究杂志出版内容重点：干细胞；骨髓干细胞；造血干细胞；脂肪干细胞；肿瘤干细胞；胚胎干细胞；脐带脐血干细胞；干细胞诱导；干细胞分化；组织工程

Key words: Stem Cells, Myocardium, Connexins, Angiotensin II, Transforming Growth Factor beta1, Tissue Engineering

CLC Number:

R394.2

Yan Ping, Hou Jing-ying, Zheng Shao-xin, Long Hui-bao, Zhong Ting-ting, Zhou Chang-qing, Guo Tian-zhu, Wu Quan-hua, Wang Tong. Cardiac stem cells improve the electrophysiological stability and ventricular fibrillation threshold via ANGII/AT1R/TGF-beta1/SMAD/CX43 signaling pathway[J]. Chinese Journal of Tissue Engineering Research, 2016, 20(28): 4226-4233.

Figures/Tables 2

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