Document Detail


Long-term IGF-I exposure decreases autophagy and cell viability.
MedLine Citation:
PMID:  20830296     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A reduction in IGF-I signaling has been found to increase lifespan in multiple organisms despite the fact that IGF-I is a trophic factor for many cell types and has been found to have protective effects against multiple forms of damage in acute settings. The increase in longevity seen in response to reduced IGF-I signaling suggests that there may be differences between the acute and chronic impact of IGF-I signaling. We have examined the possibility that long-term stimulation with IGF-I may have a negative impact at the cellular level using quiescent human fibroblasts. We find that fibroblast cells exposed to IGF-I for 14 days have reduced long-term viability as judged by colony forming assays, which is accompanied by an accumulation of senescent cells. In addition we observe an accumulation of cells with depolarized mitochondria and a reduction in autophagy in the long-term IGF-I treated cultures. An examination of mice with reduced IGF-I levels reveals evidence of enhanced autophagy and fibroblast cells derived from these mice have a larger mitochondrial mass relative to controls indicating that changes in mitochondrial turnover occurs in animals with reduced IGF-I. The results indicate that chronic IGF-I stimulation leads to mitochondrial dysfunction and reduced cell viability.
Authors:
Alessandro Bitto; Chad Lerner; Claudio Torres; Michaela Roell; Marco Malaguti; Viviana Perez; Antonello Lorenzini; Silvana Hrelia; Yuji Ikeno; Michelle Elizabeth Matzko; Roger McCarter; Christian Sell
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-09-07
Journal Detail:
Title:  PloS one     Volume:  5     ISSN:  1932-6203     ISO Abbreviation:  PLoS ONE     Publication Date:  2010  
Date Detail:
Created Date:  2010-09-10     Completed Date:  2011-02-18     Revised Date:  2013-05-28    
Medline Journal Info:
Nlm Unique ID:  101285081     Medline TA:  PLoS One     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e12592     Citation Subset:  IM    
Affiliation:
Department of Pathology, Drexel University College of Medicine, Philadelphia, Pennsylvania, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis
Autophagy*
Cell Survival
Cells, Cultured
Fibroblasts / cytology*,  metabolism*
Insulin-Like Growth Factor I / metabolism*
Mice
Mitochondria / metabolism
Grant Support
ID/Acronym/Agency:
AG022443/AG/NIA NIH HHS
Chemical
Reg. No./Substance:
67763-96-6/Insulin-Like Growth Factor I
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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