MicroRNA-361 regulates apoptosis of cardiomyocytes after ischemic-reperfusion injury.

Abstract

To investigate the role and mechanism of microRNA-361 (miR-361) in apoptosis after myocardial ischemia-reperfusion (MI-R) injury. For the in vivo experiments, the mice model of MI-R injury was established, and miR-361 was up-regulated via lentivirus with miR-298 overexpression. The expression of miR-361 and Bcl-2 associated X protein (BAX) were detected via Real Time-quantitative Polymerase Chain Reaction (qPCR) and Western blot (WB), respectively. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay was used to detect the apoptosis in myocardial tissues. MI-R injury was also simulated in vitro experiments, and the relationship between miR-361 and BAX was verified using Luciferase reporter vector. The effect of miR-361 on cardiomyocyte apoptosis was also detected at the cellular level. In vivo experiments showed that the miR-361 expression was down-regulated at MI-R injury area. The up-regulation of miR-361 significantly decreased the expression of BAX, reduced the myocardial apoptosis and inhibited the mitochondrial apoptosis pathway protein expression, including the cytochrome-c (Cyt-C) and cleaved caspase-3. In vitro experiments revealed that BAX was a target gene of miR-361 and further proved that miR-361 could inhibit the cytochrome-c and cleaved caspase-3 expression, as well as reduce the myocardial apoptosis through BAX. MiR-361 could improve the myocardial apoptosis through the target gene BAX in MI-R injury.