Document Detail

Autophagy plays a protective role in free cholesterol overload-induced death of smooth muscle cells.
MedLine Citation:
PMID:  20484746     Owner:  NLM     Status:  MEDLINE    
Smooth muscle cells (SMC) make up most of the vascular system. In advanced atherosclerotic plaques, dying SMCs undergo a complex death mode. In the present study, we examined the activation of autophagy in SMCs overloaded with excess free cholesterol (FC) and investigated the possible role which autophagy plays during the FC-induced cell death. After incubation with excess FC, a robust expression of autophagic vacuoles (AV) was detected using both fluorescence microscopy and transmission electron microscopy (TEM). The results revealed that FC induced a time-dependent upregulation of microtubule-associated protein-1 light chain 3-II (LC3-II). Inhibition of autophagy by 3-methyladenine (3-MA) enhanced both cell apoptosis and necrosis, while on the contrary, rapamycin inhibited cell death following cholesterol application. Furthermore, the impact of the colocalization of fragmented mitochondria with AVs was observed after cholesterol treatment. Our results also revealed that the modulation of autophagy directly influenced the cellular organellar stress. In conclusion, our findings demonstrated that excess FC induced the activation of autophagy in SMCs as a cellular defense mechanism, possibly through the degradation of dysfunctional organelles such as mitochondria and endoplasmic reticulum.
Kedi Xu; Yi Yang; Ming Yan; Jianan Zhan; Xiao Fu; Xiaoxiang Zheng
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-05-19
Journal Detail:
Title:  Journal of lipid research     Volume:  51     ISSN:  0022-2275     ISO Abbreviation:  J. Lipid Res.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-08-12     Completed Date:  2011-02-14     Revised Date:  2011-09-13    
Medline Journal Info:
Nlm Unique ID:  0376606     Medline TA:  J Lipid Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2581-90     Citation Subset:  IM    
Department of Biomedical Engineering, Key Laboratory of Biomedical Engineering of Ministry of Education, Zhejiang University, Hangzhou, China.
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MeSH Terms
Autophagy / physiology*
Cell Death / physiology*
Cholesterol / blood*
Endoplasmic Reticulum / metabolism
Mitochondria / metabolism
Myocytes, Smooth Muscle / cytology,  pathology*,  physiology*
Rats, Sprague-Dawley
Vacuoles / metabolism,  ultrastructure
Reg. No./Substance:

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