alexa Upregulation of Autophagy by Angiotensin II Triggers Phenotypic Switching of Aortic Vascular Smooth Muscle Cells
ISSN: 2155-9880

Journal of Clinical & Experimental Cardiology
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Research Article

Upregulation of Autophagy by Angiotensin II Triggers Phenotypic Switching of Aortic Vascular Smooth Muscle Cells

Yangfeng Tang, Zilin Liao, Zhiyun Xu* and Lin Han
Department of Cardiothoracic Surgery, Changhai Hospital of the Second Military Medical College Shanghai, China
Corresponding Author : Zhiyun Xu
Department of Cardiothoracic Surgery, Changhai Hospital
the Second Military Medical College Shanghai, 200433, China
Tel: +8615800629181
Fax: +8621-65490979
E-mail: [email protected]
Received March 24, 2014; Accepted April 25, 2014; Published May 10, 2014
Citation: Tang Y, Liao Z, Xu Z, Han L (2014) Upregulation of Autophagy by Angiotensin II Triggers Phenotypic Switching of Aortic Vascular Smooth Muscle Cells. J Clin Exp Cardiolog 5:308. doi:10.4172/2155-9880.1000308
Copyright: © 2014 Tang Y, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Background: Angiotension II (AngII) has important roles on Vascular Smooth Muscle Cell VSMC) biological functions. It has been indicated to promote the synthetic phenotype of VSMC, but the underlying mechanism is still needed to be elucidated.

Methods and Results: In this study, we found AngII infusion promotes a increased form of autophagy characterized by increased expression of Beclin1 and LC3-II in the cultured human aortic vascular smooth muscle cells. The growth of autophagy stimulated by AngII could enhance implication of synthetic proteins in VSMCs, while inhibition of autophagy with spautin-1or 3-MA can encourage the stability of the contractile phenotype in AngIItreated VSMCs.

Conclusion: These results suggest that up regulation of autophagy by AngII contributes to the increase of synthetic phenotype, which triggered the functional change in VSMCs.

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