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.
Keywords: Cardiomyocyte cell; Hypoxia and reoxygenation; Inflammatory response; Molecular mechanism; Myocardial injury.