MiR-708-3p Alleviates Inflammation and Myocardial Injury After Myocardial Infarction by Suppressing ADAM17 Expression

MicroRNAs (miRNAs) emerge as important regulators for myocardial infarction (MI). However, the function of miR-708-3p during MI is unclear. H9c2 cells were cultured in a hypoxic environment and Sprague-Dawley rats experienced surgical ligation of the left anterior descending coronary artery to establish MI models. qPCR was used to measure the expression level of miR-708-3p and ADAM17 mRNA. ELISA was used to detect inflammatory cytokines TNF-alpha, IL-6, and IL-1 beta, and myocardial injury markers LDH, CK-MB, and cTnI. Cell apoptosis and viability were monitored by flow cytometry analysis and MTT assay. ADAM17 expression was detected by Western blot. Dual-luciferase reporter gene experiments were carried out to identify binding sites between miR-708-3p and ADAM17 3'UTR. In vivo, left ventricle functions and myocardial remodeling of the rats were measured by echocardiography. MiR-708-3p was found to be significantly decreased in H9c2 cells after hypoxia induction and in heart tissues of rats with MI or serum samples of patients with MI, while ADAM17 was upregulated. Overexpression of miR-708-3p inhibited inflammation and injury of H9c2 cells cultured in hypoxia and the heart of the rats with MI. ADAM17 was verified as a direct target of miR-708-3p and restoration of ADAM17 reversed the effects of miR-708-3p. MiR-708-3p alleviated the inflammation and injury of cardiomyocytes via targeting ADAM17.