miR-126-5p regulates H9c2 cell proliferation and apoptosis under hypoxic conditions by targeting IL-17A.

Accumulating evidence has indicated that microRNAs (miRNAs/miRs) regulate the occurrence and development of various diseases, including diabetes, osteoporosis and cardiovascular conditions. However, the role of miRNAs in acute myocardial infarction (AMI) is not completely understood. The present study aimed to evaluate the therapeutic efficacy and mechanisms underlying the effects of miR-126-5p on H9c2 cell proliferation and apoptosis by targeting interleukin (IL)-17A. A total of 40 patients with AMI and 40 healthy volunteers were recruited in the present study and the expression levels of serum miR-126-5p and IL-17A were determined. Following confirmation that IL-17A was a target of miR-126-5p via a dual-luciferase reporter assay, H9c2 cells were exposed to hypoxic conditions. H9c2 cell viability and apoptosis were subsequently assessed. Additionally, the protein expression levels of apoptosis-associated proteins were detected following transfection. Compared with healthy individuals, miR-126-5p expression was significantly decreased in the serum samples of patients with AMI, whereas IL-17A, the target of miR-126-5p, was significantly increased. Following hypoxic treatment, miR-126-5p overexpression enhanced H9c2 cell viability compared with the NC group, which was subsequently reversed following co-transfection with pcDNA3.1-IL-17A. Additionally, the results indicated that hypoxia-induced H9c2 cell apoptosis was significantly reduced following transfection with miR-126-5p mimics via the PI3K/AKT signaling pathway compared with the NC group. The present study indicated that miR-126-5p may serve as a novel miRNA that regulates H9c2 cell viability and apoptosis by targeting IL-17A under hypoxic conditions. Therefore, miR-126-5p may serve as a crucial biomarker for the diagnosis of AMI.