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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 3018190, 9 pages
Research Article

Moderate Autophagy Inhibits Vascular Smooth Muscle Cell Senescence to Stabilize Progressed Atherosclerotic Plaque via the mTORC1/ULK1/ATG13 Signal Pathway

1Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, China
2Training and Postgraduate Management Department, Medical Administrative Division, Chinese PLA General Hospital, Beijing 100853, China
3Department of Cardiology, Chinese PLA General Hospital, Beijing 100853, China

Correspondence should be addressed to Feng Cao; moc.361@8288oacgnef and Yabin Wang; moc.361@2028byw

Received 15 November 2016; Revised 15 January 2017; Accepted 21 February 2017; Published 21 June 2017

Academic Editor: Anindita Das

Copyright © 2017 Zhenli Luo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


In order to investigate the effects of autophagy induced by rapamycin in the development of atherosclerosis plaque we established murine atherosclerosis model which was induced in ApoE−/− mice by high fat and cholesterol diet (HFD) for 16 weeks. Rapamycin and 3-Methyladenine (MA) were used as autophagy inducer and inhibitor respectively. The plaque areas in aortic artery were detected with HE and Oil Red O staining. Immunohistochemical staining were applied to investigate content of plaque respectively. In contrast to control and 3-MA groups, rapamycin could inhibit atherosclerosis progression. Rapamycin was able to increase collagen content and a-SMA distribution relatively, as well as decrease necrotic core area. Then we used MOVAS and culture with ox-LDL for 72 h to induce smooth muscle-derived foam cell model in vitro. Rapamycin and 3-MA were cultured together respectively. Flow cytometry assay and SA-β-Gal staining experiments were performed to detect survival and senescence of VSMCs. Western blot analysis were utilized to analyze the levels of protein expression. We found that rapamycin could promote ox-LDL-induced VSMCs autophagy survival and alleviate cellular senescence, in comparison to control and 3-MA groups. Western blot analysis showed that rapamycin could upregulate ULK1, ATG13 and downregulate mTORC1 and p53 protein expression.