BACKGROUND: Acute myocardial infarction (AMI) is a severe disease causing heart failure and sudden death. Studies indicate that microRNAs (miRNAs) are involved in the pathophysiology of AMI. In the present study, we carefully explored the effects of miR-122 on myocardial hypoxia injury and its possible underlying mechanism.

MATERIAL AND METHODS: miR-122 expression was analyzed in H9c2 cardiomyocytes after being transfected with miR-122 mimic, ASO-miR-122, or negative control. Cell viability and apoptosis were investigated by CCK-8 assays and flow cytometry analysis, respectively. Cell migration was analyzed using wound-healing assays. Western blotting was performed to analyze the expression of phosphatase and tensin homolog deleted on chromosome 10 (PTEN)/phosphatidylinositol 3-hydroxy kinase (PI3K)/AKT and LC3-II/LC3-I.

RESULTS: Hypoxia exposure significantly inhibited H9c2 cell viability (P<0.01). miR-122 overexpression promoted the hypoxia-induced H9c2 cell proliferation and migration loss (P<0.05), and cell apoptosis was increased (P<0.05). miR-122 knockdown enhanced cell viability and decreased cell apoptosis (P<0.05). Knockdown of miR-122 enhanced PTEN/PI3K/AKT activation and cell autophagy. Overexpression of miR-122 inhibited the PTEN/PI3K/AKT pathway and cell autophagy pathway.

CONCLUSIONS: The expression of miR-122 is involved in hypoxia-induced H9c2 cardiomyocyte injury. Knockdown of miR-122 protects H9c2 cells from hypoxia-induced apoptosis and enhances cell viability.

Keywords: Cell Hypoxia