MiR-15a-5p accelerated vascular smooth muscle cells viabilities and migratory abilities via targeting Bcl-2.

Aortic dissection (AD) caused by the tear in the aortic wall threatens aorta, causing severe chest pain, syncope and even death. Fortunately, development of genetic technology provides promising approaches for AD treatment. To analyze impacts of miR-15a-5p on modulating cell viability and migratory ability of vascular smooth muscle cells (VSMCs). Ang II (0, 0.05 and 0.1 microM) treatment were applied for inducing inflammatory reactions of VSMCs. RNA expressions of miR-15a-5p with Bcl-2 was examined using RT-qPCR. CCK-8 and transwell evaluated cell viability and migratory ability, respectively. The binding about miR-15a-5p with Bcl-2 were detected by luciferase reporter assay. Western blot detected protein expressions of Bcl-2, MCP-1 and MMP-9. Ang II treatment not only accelerated VSMCs viability and migratory abilities, but also upregulated MCP-1 and MMP-9 protein expressions. MiR-15a-5p was detected to be promoted by Ang II. However, miR-15a-5p inhibitor decreased VSMC cell viability and migratory ability and suppressed protein expressions of MCP-1 and MMP-9. Bcl-2 was targeted and downregulated by miR-15a-5p. Nevertheless, high VSMC cell viability and migration caused by miR-15a-5p overexpression were hindered with overexpressed Bcl-2. MiR-15a-5p mimics also elevated MCP-1 and MMP-9 protein expressions, which were inhibited by Bcl-2 upregulation.