Hsa-miR-199a-5p Protect Cell Injury in Hypoxia Induces Myocardial Cells Via Targeting HIF1α.

Abstract

Myocardial infarction (MI) is one of the most common global diseases. Recently, microRNA 199a-5p (miR-199a-5p) has been recognized as a vital regulator in several human diseases. Nevertheless, the function of miR-199a-5p and the associated downstream molecular mechanisms in myocardial injury remain undescribed. Here, we assessed the relative expression of miR-199a-5p in an oxidative stress injury model of human myocardial cells. The effects of miR-199a-5p on myocardial cell viability were determined by cell counting kit-8 (CCK-8), terminal deoxynucleotidyl transferase UTP nick end labeling (TUNEL), flow cytometry, and western blot assays. Online bioinformatic analysis was used to predict the aim of miR-199a-5p in cardiomyocyte injury, which was confirmed by dual-luciferase reporter assays. miR-199a-5p increased the growth rate of cardiomyocytes after treatment with a hypoxic environment. miR-199a-5p acted as an inhibitor directly targeted hypoxia-inducible factor-1 (HIF1α) expression, which was higher in the cardiomyocyte injury model than that in healthy myocardial cells. Upregulated HIF1α expression abolished miR-199a-5p-induced cell proliferation in the cardiomyocyte hypoxia model. Our results suggest that miR-199a-5p is a potential prognostic biomarker in myocardial damage.