Overexpressing MicroRNA-150 Improves Cardiac Fibrosis And Cardiac Function In Rat With Myocardial Infarction

ObjectiveAcute myocardial infarction is a disease of the highest mortality in the world.Myocardial fibrosis after myocardial infarction is an important factor causing heart failure.MicroRNA is a non-coding RNA that regulates gene expression and is closely related to acute myocardial infarction.The aim of this study was to investigate the expression of miRNA-150 in myocardium of rats with myocardial infarction and to further study the effect of miR-150 on myocardial fibrosis and cardiac function after myocardial infarction.MethodsA rat model of myocardial infarction was induced by ligating the left anterior descending artery and the overexpressing microRNA-150 or blank lentivirus vector was used to study the role of microRNA-150 in post-infarction myocardial fibrosis.Real-time PCR was used to quantitate microRNA-150 and the mRNA of collagen1?1and ?-SMA.The Western blotting was used to evaluate the expression of collagen1?1 and ?-SMA protein.The heart echocardiography and Masson colorationwas applied to measure cardiac function and myocardial fibrosis respectively.ResultsMicroRNA-150 was down-regulated in infarcted border myocardium of model rats in 28 day after ligating the left anterior descending artery(P < 0.05).Overexpressing miRNA-150 protected MI rats from myocardial fibrosis,improved myocardial infarction rats' cardiac function and inhibited the expression of collagen1?1 and ?-SMA(P<0.001).ConclusionsMicroRNA-150 is down-regulated in infarcted border myocardium of model rats.Overexpressing miR-150 promotes myocardial fibrosis and heart function after myocardial infarction.