The present study investigated the effects of micro (mi)RNA-145 on acute myocardial infarction (AMI) and the potential underlying mechanism. A total of 6 AMI and 6 normal rat tissues were investigated for the present study. It was demonstrated that miRNA-145 expression was downregulated in the AMI rat model, compared with the control group. Downregulation of miRNA-145 increased cardiac cell apoptosis, suppressed phosphorylated (p)-RAC-γ serine/threonine-protein kinase (Akt3) and p-mechanistic target of rapamycin (mTOR) protein expression levels and suppressed autophagy in an in vitr model of AMI. However, overexpression of miRNA-145 decreased cardiac cell apoptosis, induced p-Akt3 and p-mTOR protein expression and promoted autophagy in the in vitr model of AMI. The inhibition of Akt3 (GSK2110183, 1 nM) decreased the effect of the miRNA-145 upregulation on cell apoptosis in the in vitr model of AMI. Chloroquine diphosphate (5 µM) inhibited the regulatory effect of miRNA-145 upregulation on autophagy to adjust cell apoptosis, in the in vitr model of AMI. The results of the present study demonstrate that miRNA-145 inhibits myocardial infarction-induced apoptosis via autophagy associated with the Akt3/mTOR signaling pathway in viv and in vitro.

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MicroRNAs (miRs) are widely reported to be novel biomarkers involved in the process of coronary atherosclerosis (CAS). Hence, this study aims to explore the function of miR-383-3p targeting IL1R2 on inflammatory injury of coronary artery endothelial cells (CAECs) in CAS. The underlying regulatory mechanisms of miR-383-3p were analyzed in concert with the treatment of miR-383-3p mimics, miR-383-3p inhibitors, and the combination of miR-383-3p inhibitors and siRNA against IL1R2 in homocysteine (HCY)-induced CAECs. MTT, Hoechst 33258 staining, and tube formation assay were employed in order to measure cell viability, apoptosis, and tube formation, respectively. The levels of IL-1β, IL-6, IL-10, and IL-18 were determined by ELISA. IL1R2 was verified as the target gene of miR-383-3p by dual-luciferase reporter gene assay. MiR-383-3p was down-regulated in myocardial tissues of AS rats while IL1R2 was the reciprocal. The up-regulation of miR-383-3p decreased the levels of IL1R2, caspase-1, IL-1β, IL-6, and IL-18 expressions, as well as cell apoptosis rate in the HCY-induced CAECs, while IL-10 expression, cell viability, and tube formation ability were increased. These results were contraindicated in the HCY-induced CAECs treated by miR-383-3p inhibitors. In conclusion, miR-383-3p mediating IL1R2 prevents HCY-induced apoptosis and inflammation injury in CAECs through the inhibition of the activation of inflammasome signaling pathway. These findings highly indicate that miR-383-3p may be beneficial in the prevention of CAS and other cardiovascular diseases.