Conclusion
In conclusion, the overexpression of miR-136-3p could potentially impede myocardial injury in vitro and in vivo in CAD through the blockade of the Rho A/ROCK signaling pathway, highlighting a potential miR-136-3p functional relevance in the treatment of CAD.
Methods
Initially, CAD models were induced in rats by high-fat diet and intraperitoneal injection of pituitrin. Next, the effect of overexpressed miR-136-3p on cardiac function and pathological damage in myocardial tissue, cardiomyocyte apoptosis, oxidative stress and inflammatory response were assessed in CAD rats. Rat cardiac microvascular endothelial cells (CMECs) were isolated and cultured by the tissue explant method, and the CMEC injury model was induced by homocysteine (HCY). The function of miR-136-3p in vitro was further evaluated.
Objective
Coronary artery disease (CAD) is a cardiovascular disease that poses a fatal threat to human health, and the identification of potential biomarkers may help to delineate its pathophysiological mechanisms. Accumulating evidence has implicated microRNAs (miRNAs) in the pathogenesis and development of cardiovascular diseases. The present study aims to identify the expression of miRNA-136-3p (miR-136-3p) in CAD and further investigate its functional relevance in myocardial injury both in vitro and in vivo.
Results
miR-136-3p was poorly expressed in the myocardial tissue of CAD rats and CMEC injury models. In vivo assays indicated that overexpressed miR-136-3p could improve cardiac function and alleviate pathological damage in myocardial tissue, accompanied by reduced oxidative stress and inflammatory response. Moreover,in vitro assays suggested that overexpression of miR-136-3p enhanced proliferation and migration while inhibiting apoptosis of HCY-stressed CMECs. Notably, we revealed that EIF5A2 was a target gene of miR-136-3p, and miR-136-3p inhibited EIF5A2 expression and activation of the Rho A/ROCK signaling pathway.