Upregulated miR-486 Induces Therapeutic Angiogenesis and Improves Infarction Recovery in Rat Myocardial Ischemia Model

Abstract BackgroundBesides hematopoietic cells, miR-486 is also enriched in cardiac, skeletal, and smooth muscles. However, its roles in regulating the function of cardiomyocytes and tissue repair in myocardial infarction have not been explored yet.MethodsWe investigated the effects of miR-486 on the survival and hypoxic response of cardiomyocytes. Also, using adenovirus-mediated overexpression, we evaluated its therapeutic effects in myocardial repair in a rat acute myocardial infarct (AMI) model.ResultsHypoxia treatment upregulated miR-486 in cardiomyocytes. Moreover, adenovirus-mediated overexpression of miR-486 reduced cell injury, increased cell viability, and decreased apoptosis in hypoxic conditions. In a rat AMI model, administration of Ad-miR-486 reduced infarct size and collagen deposition, increased vessel density, and improved cardiac function. Furthermore, in vivo data suggest that the protective effects of miR-486 in cardiomyocytes were related to its anti-apoptotic function.ConclusionmiR-486 overexpression protects myocytes from hypoxia-induced apoptosis and has therapeutic potential in myocardial infarction.