机构：[1]Department of Cardiothoracic Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, No. 321 Zhongshan Road, Nanjing 210008, Jiangsu Province, PR China[2]Department of Cardiology, Shenzhen University General Hospital, Shenzhen 518000, Guangdong Province, PR China深圳大学总医院深圳市康宁医院深圳医学信息中心[3]Puyang Medical College, Shangyang Road and Wenyan Street, Puyang 457000, Henan Province, PR China[4]Second Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing 210023, Jiangsu Province, PR China[5]Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Road, Wuhan 430030, Hubei Province, PR China华中科技大学同济医学院附属同济医院[6]Department of Geratology, The First Affiliated Hospital, Zhejiang University College of Medicine, Hangzhou 310003, Zhejiang Province, PR China浙江大学医学院附属第一医院
Background: Mesenchymal stem cells (MSCs) are under consideration for myocardial ischemia-reperfusion (I/R) injury therapy, but their mechanism remains to be evaluated. In this article, we aimed to study the effects of the miR-29a/follistatin-like 1 axis in bone marrow-derived mesenchymal stem cells on modulating myocyte apoptosis after hypoxia-reoxygenation (H/R) injury. Methods: An in vitro myocardial ischemia-reperfusion injury model of H9c2 cells was developed by hypoxia-reoxygenation injury. The mRNA levels of follistatin-like 1, Bcl-2, Bax, and miR-29a and the protein levels of Bcl-2, Bax, cleaved caspase-3, and components of the JAK2/STAT3 pathway were detected by qRT-PCR and western blotting, respectively. Secretion of follistatin-like 1 was evaluated by enzyme-linked immunosorbent assay. Cell apoptosis was evaluated by flow cytometry. The interaction between miR-29a and follistatin-like 1 was evaluated by dual luciferase reporter assay. Results: MiR-29a suppressed the expression and secretion of follistatin-like 1 in bone marrow-derived mesenchymal stem cells. Overexpression of follistatin-like 1 in bone marrow-derived mesenchymal stem cells decreased apoptosis of myocytes induced by hypoxia-reoxygenation. Cell apoptosis in myocytes was promoted by conditioned medium from bone marrow-derived mesenchymal stem cells with ectopic miR-29a expression. Conditioned medium of miR-29a-overexpressing bone marrow-derived mesenchymal stem cells inhibited the JAK2/STAT3 pathway in myocytes to promote apoptosis of myocytes. Conclusions: MiR-29a in bone marrow-derived mesenchymal stem cells inhibits follistatin-like 1 secretion and promotes myocyte apoptosis by suppressing the JAK2/STAT3 pathway in hypoxia-reoxygenation injury. (C) 2019 Elsevier Inc. All rights reserved.
第一作者机构：[1]Department of Cardiothoracic Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, No. 321 Zhongshan Road, Nanjing 210008, Jiangsu Province, PR China
共同第一作者：
通讯作者：
通讯机构：[2]Department of Cardiology, Shenzhen University General Hospital, Shenzhen 518000, Guangdong Province, PR China[*1]Department of Cardiology, Shenzhen University General Hospital, No. 1098 Xueyuan Avenue, Xili University Town, Nanshan District,Shenzhen 518000, Guangdong Province, PR China.
推荐引用方式(GB/T 7714)：
Li Kun-Sheng,Jiang Wei-Peng,Li Qiu-Chang,et al.MiR-29a in mesenchymal stem cells inhibits FSTL1 secretion and promotes cardiac myocyte apoptosis in hypoxia-reoxygenation injury[J].CARDIOVASCULAR PATHOLOGY.2020,46:doi:10.1016/j.carpath.2019.107180.
APA：
Li, Kun-Sheng,Jiang, Wei-Peng,Li, Qiu-Chang,Zhang, Hao-Wen,Bai, Yang...&Li, Hai-Ying.(2020).MiR-29a in mesenchymal stem cells inhibits FSTL1 secretion and promotes cardiac myocyte apoptosis in hypoxia-reoxygenation injury.CARDIOVASCULAR PATHOLOGY,46,
MLA：
Li, Kun-Sheng,et al."MiR-29a in mesenchymal stem cells inhibits FSTL1 secretion and promotes cardiac myocyte apoptosis in hypoxia-reoxygenation injury".CARDIOVASCULAR PATHOLOGY 46.(2020)
