Abstract

BACKGROUND MicroRNA-490-3p (miR-490-3p) plays a role in the pathogeneses of a variety of cardiovascular diseases. Bioinformatic analysis showed that miR-490-3p was down-regulated in the myocardial tissues of mice with myocardial infarction (MI). Nevertheless, the functions and mechanisms of miR-490-3p in MI remain unclear. METHODS This study used an in-vitro model to investigate the role of miR-490-3p in MI. Human cardiac myocytes (HCMs) were cultured in a hypoxic environment. 3-(4,5)-Dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide (MTT) assay and flow cytometry were used to detect cell viability and apoptosis. The expression levels of forkhead box O1 (FOXO1) and miR-490-3p were detected by quantitative real-time PCR and Western blot. The levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), lactate dehydrogenase (LDH), cardiac troponin I (cTnI) and creatine kinase MB (CK-MB) were detected by enzyme-linked immunosorbent assay (ELISA). The targeted relationship between miR-490-3p and FOXO1 3'UTR was determined by dual-luciferase reporter gene assay. RESULTS MiR-490-3p was significantly down-regulated in hypoxia-induced HCM cells, while FOXO1 was markedly up-regulated. MiR-490-3p overexpression inhibited HCM cell inflammatory responses and injury after hypoxia treatment. FOXO1 was validated to be a direct target of miR-490-3p and its overexpression weakened the effects of miR-490-3p on cell viability, apoptosis, as well as inflammatory responses. CONCLUSION MiR-490-3p alleviates cardiomyocyte injury via targeting FOXO1 in MI.