Abstract
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 β-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.
Highlights
Atherosclerosis is a common cardiovascular disease which often leads to vascular lesions, arterial intimal thickening, increased infiltration of inflammatory cells, and the formation of a lipidrich fibrous plaques [1,2]
Previous studies showed that multiple mechanisms are involved in cardiac remodeling among these, the renin–angiotensin system has been associated with the progression of cardiovascular diseases through angiotensin II (Ang II), which acts as a growth factor regulating cardiovascular homeostasis and blood volume [4]
This study found that the overexpression of miR-134 significantly increased the expressions of cellular antioxidant factors, thereby protecting human aortic smooth muscle cells (HASMCs) from Ang II-induced cardiac dysfunction via the Akt/mechanistic target of rapamycin (mTOR) pathway
Summary
Atherosclerosis is a common cardiovascular disease which often leads to vascular lesions, arterial intimal thickening, increased infiltration of inflammatory cells, and the formation of a lipidrich fibrous plaques [1,2]. The presence of atherosclerosis influence coronary arteries due to the build-up of plaque. Vascular smooth muscle cell (VSMC) dysfunction plays an important role on the pathogenesis of cardiovascular disease[3]. Previous studies showed that multiple mechanisms are involved in cardiac remodeling among these, the renin–angiotensin system has been associated with the progression of cardiovascular diseases through angiotensin II (Ang II), which acts as a growth factor regulating cardiovascular homeostasis and blood volume [4]. Angiotensin II is involved in regulating migration, proliferation and hypertrophy in VSMCs [5]. Angiotensin II can induce the activation of calcineurin and the mitochondria-
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