MicroRNA-27a regulates angiotensin II-induced vascular smooth muscle cell proliferation and migration by targeting α-smooth muscle-actin in vitro.

Angiotensin II (Ang II) modulates VSMCs phenotypic switch that play a critical role in the cardiovascular diseases. MicroRNA-27a (miR-27a) has been proven to be involved in regulating vascular remodeling; however, the functional role of miR-27a in VSMCs in response to Ang II stimulation need to be elucidated. Cell proliferation and migration were measured by Cell counting kit-8 (CCK-8), BrdU incorporation and scratch wound assay in VSMCs transfected with miR-27a or its inhibitor. The target of miR-27a was confirmed using bioinformatics analysis and luciferase reporter assay. Ang II treatment time-dependently increased proliferation and migration of VSMCs accompanied with downregulation of α-smooth muscle-actin (α-SMA) and upregulation of miR-27a expression. Moreover, knockdown of miR-27a in VSMCs significantly attenuated Ang II-induced cell proliferation and migration, whereas this effect was aggravated by overexpression of miR-27a. A potential mechanistic analysis revealed that miR-27a directly targeted α-SMA, which mediated miR-27a-induced cell proliferation and migration. In conclusion, these results indicate that miR-27a acts as a novel regulator of Ang II-induced proliferation and migration by directly targeting α-SMA expression in VSMCs in vitro, and may be a potential therapeutic target for treating vascular diseases.