Department of Cardiology, The Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu, China.
Anatol J Cardiol. 2022 May;26(5):373-381. doi: 10.5152/AnatolJCardiol.2021.901.
Myocardial infarction, a coronary heart disease, is a serious hazard to human health. Cardiomyocyte oxidative stress and apoptosis have been considered as the main causes of myocardial infarction. Here, we aimed to investigate the role of miR-615-3p in oxidative stress and apoptosis of human cardiomyocytes.
Reverse transcription-quantitative polymerase chain reaction was performed to determine miR-615-3p or MEF2A expression in human cardiomyocytes. Apoptosis and viability of human cardiomyocytes were assessed by flow cytometry analysis and CCK-8 assay. In addition, the contents of malondialdehyde, reactive oxygen species, and superoxide dismutase were detected by corresponding commercial kits. The binding of miR-615-3p and MEF2A in human cardiomyocytes was examined by luciferase reporterassay.
Hypoxia/reoxygenation treatment downregulated the expression level ofmiR-615-3p in human cardiomyocytes. Overexpressing miR-615-3p increased human cardiomyocyte viability and decreased human cardiomyocyte apoptosis. Moreover, miR- 615-3p mimics suppressed oxidative stress in hypoxia/reoxygenation-stimulated human cardiomyocytes. MEF2A was confirmed as a target gene of miR-615-3p and was highly expressed in hypoxia/reoxygenation-stimulated human cardiomyocytes, and its upregu-lation partially reversed the influence of miR-615-3p mimics on oxidative stress and apop-tosis of human cardiomyocytes. Moreover, miR-615-3p inactivated the P13K/Akt pathway by inhibiting MEF2A.
Overexpression of miR-615-3p protects human cardiomyocytes from oxida-tive stress injury by targeting MEF2A via the PI3K/Akt signaling.
心肌梗死是一种冠心病，严重危害人类健康。心肌细胞氧化应激和细胞凋亡被认为是心肌梗死的主要原因。在这里，我们旨在研究 miR-615-3p 在人心肌细胞氧化应激和细胞凋亡中的作用。
采用反转录定量聚合酶链反应检测人心肌细胞中 miR-615-3p 或 MEF2A 的表达。通过流式细胞术分析和 CCK-8 测定评估人心肌细胞的凋亡和活力。此外，通过相应的商业试剂盒检测丙二醛、活性氧和超氧化物歧化酶的含量。通过荧光素酶报告实验检测 miR-615-3p 与人心肌细胞中 MEF2A 的结合。
缺氧/复氧处理下调了人心肌细胞中 miR-615-3p 的表达水平。过表达 miR-615-3p 增加了人心肌细胞的活力，减少了人心肌细胞的凋亡。此外，miR-615-3p 模拟物抑制了缺氧/复氧刺激的人心肌细胞中的氧化应激。MEF2A 被证实是 miR-615-3p 的靶基因，在缺氧/复氧刺激的人心肌细胞中高表达，其上调部分逆转了 miR-615-3p 模拟物对人心肌细胞氧化应激和凋亡的影响。此外，miR-615-3p 通过抑制 MEF2A 使 P13K/Akt 通路失活。
miR-615-3p 通过靶向 MEF2A 抑制 PI3K/Akt 信号通路，对人心肌细胞氧化应激损伤具有保护作用。
