MicroRNA-127-3p Inhibits Cardiomyocyte Inflammation and Apoptosis after Acute Myocardial Infarction via Targeting CDKN3.

Abstract

Given the potential role of microRNA (miRNA) in the pathological process of ischemic heart disease, clinical patients with acute myocardial infarction (AMI) were recruited and serum miR-127-3p levels in the patients were tested. In vitro, the effects of miR-127-3p on cardiomyocyte apoptosis and inflammation induced by hypoxia and reoxygenation (H/R) were also elucidated in AC16 cells.Collection of serum samples from 113 AMI patients and 104 healthy controls was done. Human cardiomyocyte cell line AC16 was exposed to the H/R condition for the cell function experiments. qRT-PCR was applied for mRNA detection, and cell viability and apoptosis were evaluated. To assess inflammatory response, an enzyme-linked immunosorbent assay was carried out. For the target gene analysis, luciferase reporter assay was accomplished.MiR-127-3p was significantly reduced in the serum of AMI patients, which was negatively correlated with CDKN3 mRNA levels. Serum miR-127-3p was negatively correlated with Scr, cTnI, CK-MB, IL-6, and TNF-α. CDKN3 serves as a target gene of miR-127-3p, its mRNA levels were reduced by miR-127-3p overexpression. H/R treatment caused the suppression of cell viability and the promotion of cell apoptosis, which was changeover by miR-127-3p overexpression. Furthermore, MiR-127-3p overexpression inhibited cell inflammatory response. The rescue experiments revealed that CDKN3 overexpression canceled the protective influence of miR-127-3p against cardiomyocyte injury and inflammatory response.MiR-127-3p can alleviate AMI-induced cardiomyocyte apoptosis and cardiac dysfunction, which is related to its anti-inflammatory effect and its downstream CDKN3 gene.