Role of miR-134 in angiotensin II-induced vascular cell pathological changes in atherosclerosis

Purpose: To investigate the role of miR-134 in vascular smooth muscle cell dysfunction-related cardiovascular disease. Methods: The effect of miR-134 was evaluated after human aortic smooth muscle cells (HASMCs) were transfected with miR-134 mimics. The expression levels of p-Akt, mechanistic target of rapamycin (mTOR), cleaved caspase-3, p53, and beta-actin were evaluated by immunoblotting. Terminal deoxynucleotidyl transferase dUTP nick-end labeling was used to measure cell apoptosis. Reactive oxygen species levels were assayed by fluorescence microscopy after staining with 2', 7'-dichlorofluorescein diacetate. Results: Angiotensin II treatment induced miR-134 expression and Akt/mTOR activation, and inhibited cell viability in HASMCs (p < 0.01). Co-treatment with miRNA-134 reversed Ang II-induced HASMC dysfunction (p < 0.01). Overexpression of miR-134 is protective in Ang II-induced oxidative stress and apoptosis via the Akt/mTOR pathway (p < 0.05). Conclusion: MicroRNA-134 in HASMCs is a potential therapeutic target for preventing Ang II-induced cardiac dysfunction via modulating Akt/mTOR pathway.