Abstract
Human vascular smooth muscle cells (hVSMCs) are crucial in the progression of coronary heart disease (CHD). The present study aimed to investigate the role of microRNA-208a-3p (miR-208a-3p) in hVSMCs. Reverse transcription quantitative-PCR was performed to detect the levels of miR-208a-3p in the peripheral blood samples of patients with CHD and healthy volunteers. The results showed that miR-208a-3p was significantly upregulated in peripheral blood samples from patients with CHD compared with in healthy volunteers. Bioinformatics analysis and dual-luciferase reporter assays indicated that B-cell translocation gene 1 (BTG1) was a direct target gene of miR-208a-3p, and was downregulated in the peripheral blood samples of patients with CHD. Furthermore, this study also suggested that miR-208a-3p served an inhibitory role in the proliferation of hVSMCs, induced cell apoptosis, promoted the protein expression of Bax and reduced Bcl-2 protein expression; however, these effects were reversed by BTG1 silencing. In addition, the role of the PI3K/AKT pathway in mediating hVSMC apoptosis was examined via western blot analysis. Results indicated that inhibition of miR-208a-3p decreased phosphorylated (p)-AKT protein expression levels and the ratio of p-AKT/AKT in hVSMCs; however, BTG1-small interfering RNA abolished these effects. Taken together, these findings revealed that miR-208a-3p served a critical role in CHD development, regulating hVSMC function via targeting of BTG1, which was associated with the PI3K/AKT signaling pathway. Therefore, downregulated miR-208a-3p may serve as an ideal therapeutic target for CHD diagnosis and therapy.