Document Detail


Autophagy activation in the injured photoreceptor inhibits fas-mediated apoptosis.
MedLine Citation:
PMID:  21421874     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE: To examine the activation of autophagy and its relationship to Fas-mediated photoreceptor apoptosis during experimental retinal detachment.
METHODS: Retina-retinal pigment epithelium (RPE) separation was created in Brown-Norway rats by subretinal injection of 1% hyaluronic acid and the intraretinal levels of the autophagy proteins LC3 and Atg5, the time course of LC3-I to LC3-II conversion, and the activation of cathepsins B and D were assayed with Western blot analysis and immunohistochemistry. We measured the ability of a Fas-activating antibody to induce LC3-I to LC3-II conversion in 661W cells, and the in vivo effect of Met12, a small molecule inhibitor of the Fas receptor, on LC3-I to LC3-II conversion and Atg5 expression. Autophagy activation was inhibited using 3-methyladenine (3-MA) or siRNA knockdown of Atg5 and the effect on apoptosis was measured using a caspase 8 activity assay, caspase 8 immunoblots, and photoreceptor TUNEL staining.
RESULTS: Retina-RPE separation resulted in a Fas-dependent activation of autophagy, with increased Atg5 levels and intraphotoreceptor conversion of LC3-I to LC3-II. Detached retinas had increased levels of autophagosome-associated lysosomal proteases, cathepsins B and D. Inhibition of autophagy by 3-MA or siAtg5 accelerated the time course of caspase 8 activation and photoreceptor TUNEL staining.
CONCLUSIONS: Autophagy activation occurs in the photoreceptors after retina-RPE separation. This appears to be, at least in part, dependent on Fas receptor activation, and plays a role in regulating the level of photoreceptor apoptosis.
Authors:
Cagri G Besirli; Nicholas D Chinskey; Qiong-Duan Zheng; David N Zacks
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-06-13
Journal Detail:
Title:  Investigative ophthalmology & visual science     Volume:  52     ISSN:  1552-5783     ISO Abbreviation:  Invest. Ophthalmol. Vis. Sci.     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-06-14     Completed Date:  2011-08-23     Revised Date:  2011-12-21    
Medline Journal Info:
Nlm Unique ID:  7703701     Medline TA:  Invest Ophthalmol Vis Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4193-9     Citation Subset:  IM    
Affiliation:
Department of Ophthalmology and Visual Sciences, W. K. Kellogg Eye Center, University of Michigan, Ann Arbor, Michigan 48105-0714, USA.
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MeSH Terms
Descriptor/Qualifier:
Adenine / analogs & derivatives,  pharmacology
Animals
Antigens, CD95 / metabolism*
Apoptosis* / drug effects
Autophagy* / drug effects
Blotting, Western
Caspase 8 / metabolism
Cathepsin B / metabolism
Cathepsin D / metabolism
Cell Line
Enzyme Activation / drug effects
Immunohistochemistry
Male
Microtubule-Associated Proteins / metabolism
Photoreceptor Cells, Vertebrate*
Protein Isoforms / metabolism
Proteins / genetics
RNA, Small Interfering / pharmacology
Rats
Rats, Inbred BN
Retinal Detachment / physiopathology*
Time Factors
Grant Support
ID/Acronym/Agency:
NEI-EY-07003/EY/NEI NIH HHS; R01 EY020823-01/EY/NEI NIH HHS; R01-020823//PHS HHS
Chemical
Reg. No./Substance:
0/Antigens, CD95; 0/Atg5 protein, rat; 0/LC3 protein, rat; 0/Microtubule-Associated Proteins; 0/Protein Isoforms; 0/Proteins; 0/RNA, Small Interfering; 5142-23-4/3-methyladenine; 73-24-5/Adenine; EC 3.4.22.-/Casp8 protein, rat; EC 3.4.22.-/Caspase 8; EC 3.4.22.1/Cathepsin B; EC 3.4.22.1/Ctsb protein, rat; EC 3.4.23.5/Cathepsin D; EC 3.4.23.5/Ctsd protein, rat

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