Coronary heart disease (CHD) is a serious condition comprising atherosclerosis-mediated ischaemic and hypoxic myocardial injury. This study aimed to investigate the mechanism of the miR-210/Casp8ap2 signalling pathway in hypoxic myocardial cells. mRNA and protein expression levels were determined by quantitative real-time PCR and western blotting, respectively. MTT was used to evaluate cell survival, and flow cytometry was used to assess apoptosis and the cell cycle distribution. The interaction between miR-210 and ­Casp8ap2 was detected by dual-luciferase reporter assay. As a result, overexpression of miR-210 significantly inhibited apoptosis and reduced the proportion of cells in G1 phase. Moreover, miR-210 suppressed autophagy by upregulating p62 levels and reducing the LC3-II/I ratio in hypoxic cardiomyocytes. miR-210 regulated apoptosis and autophagy by directly targeting Casp8ap2. Furthermore, the expression levels of Casp8ap2, Cleaved caspase 8, Cleaved caspase 3and Beclin-1 were all decreased in response to miR-210. In short, our results suggest that miR-210 exerts anti-apoptotic and anti-autophagic effects in hypoxic cardiomyocytes, which alleviates myocardial injury in response to hypoxia.
Cytogenet Genome Res

中文翻译：

---

microRNA-210/Casp8ap2 轴通过调节细胞凋亡和自噬减轻缺氧诱导的心肌损伤

冠心病 (CHD) 是一种严重的疾病，包括动脉粥样硬化介导的缺血性和缺氧性心肌损伤。本研究旨在探讨miR-210/Casp8ap2信号通路在缺氧心肌细胞中的作用机制。mRNA 和蛋白质表达水平分别通过定量实时 PCR 和蛋白质印迹确定。MTT用于评估细胞存活，流式细胞术用于评估细胞凋亡和细胞周期分布。通过双荧光素酶报告基因检测检测 miR-210 和 Casp8ap2 之间的相互作用。结果，miR-210的过表达显着抑制了细胞凋亡并降低了G1期细胞的比例。此外，miR-210 通过上调 p62 水平和降低缺氧心肌细胞中的 LC3-II/I 比率来抑制自噬。miR-210 通过直接靶向 Casp8ap2 调节细胞凋亡和自噬。此外，Casp8ap2、Cleaved caspase 8、Cleaved caspase 3和Beclin-1的表达水平均因miR-210而降低。简而言之，我们的结果表明 miR-210 在缺氧心肌细胞中发挥抗凋亡和抗自噬作用，从而缓解缺氧引起的心肌损伤。
细胞遗传基因组研究