Document Detail


Early onset senescence occurs when fibroblasts lack the glutamate-cysteine ligase modifier subunit.
MedLine Citation:
PMID:  19427898     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cellular senescence is the irreversible entry of cells into growth arrest. Senescence of primary cells in culture has long been used as an in vitro model for aging. Glutamate-cysteine ligase (GCL) controls the synthetic rate of the important cellular antioxidant glutathione (GSH). The catalytic subunit of GCL, GCLC, is catalytically active and essential for life. By contrast the modifier subunit of GCL, GCLM, is dispensable in mice. Although it is recognized that GCLM increases the rate of GSH synthesis, its physiological role is unclear. Herein, we show that loss of Gclm leads to premature senescence of primary murine fibroblasts as characterized by: (a) diminished growth rate, (b) cell morphology consistent with senescence, (c) increases in senescence-associated beta-galactosidase activity, and (d) cell cycle arrest at the G(1)/S and G(2)/M boundaries. These changes are accompanied by increased intracellular ROS, accumulation of DNA damage, and induction of p53 and p21 proteins. We also found that N-acetylcysteine increases intracellular GSH and prevents premature senescence in Gclm(-/-) cells. These results suggest that the control of GCLM, which in turn controls aspects of the cellular redox environment via GSH, is important in determining the replicative capacity of the cell.
Authors:
Ying Chen; Elisabet Johansson; Yunxia Fan; Howard G Shertzer; Vasilis Vasiliou; Daniel W Nebert; Timothy P Dalton
Related Documents :
16608398 - Mitochondrial dysfunction and cell senescence: cause or consequence?
12771028 - Inhibition of telomerase activity by geldanamycin and 17-allylamino, 17-demethoxygeldan...
9846988 - Expression of telomerase activity in human endometrium is localized to epithelial gland...
6600988 - Asbestos exposure correlates with alterations in circulating t cell subsets.
19036868 - Chloride accumulation drives volume dynamics underlying cell proliferation and migration.
16027728 - Roles of the rac1 and rac3 gtpases in human tumor cell invasion.
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2009-05-08
Journal Detail:
Title:  Free radical biology & medicine     Volume:  47     ISSN:  1873-4596     ISO Abbreviation:  Free Radic. Biol. Med.     Publication Date:  2009 Aug 
Date Detail:
Created Date:  2009-07-14     Completed Date:  2010-01-14     Revised Date:  2011-05-03    
Medline Journal Info:
Nlm Unique ID:  8709159     Medline TA:  Free Radic Biol Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  410-8     Citation Subset:  IM    
Affiliation:
Department of Environmental Health and Center for Environmental Genetics, University of Cincinnati Medical Center, Cincinnati, OH 45267-0056, USA. ying.chen@ucdenver.edu
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Acetylcysteine / pharmacology
Animals
Cell Aging / drug effects,  genetics
Cell Culture Techniques
Cell Cycle / drug effects,  genetics
Cell Growth Processes / drug effects,  genetics
Cyclin-Dependent Kinase Inhibitor p21 / genetics,  metabolism
DNA Damage
Female
Fetus
Fibroblasts / metabolism*,  pathology
Free Radical Scavengers / pharmacology
Glutamate-Cysteine Ligase / genetics,  metabolism*
Glutathione / metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
Pregnancy
Protein Subunits / genetics,  metabolism*
Reactive Oxygen Species / metabolism
Tumor Suppressor Protein p53 / genetics,  metabolism
beta-Galactosidase / metabolism
Grant Support
ID/Acronym/Agency:
P30 ES006096-10S19007/ES/NIEHS NIH HHS; P30 ES006096-159007/ES/NIEHS NIH HHS; P30 ES06096/ES/NIEHS NIH HHS; R01 ES012463/ES/NIEHS NIH HHS; R01 ES012463-01/ES/NIEHS NIH HHS; R01 ES012463-02/ES/NIEHS NIH HHS; R01 ES012463-03/ES/NIEHS NIH HHS; R01 ES012463-04/ES/NIEHS NIH HHS; R01 ES012463-05/ES/NIEHS NIH HHS; R01 EY017963/EY/NEI NIH HHS; R01 EY017963-01A1/EY/NEI NIH HHS; R01 EY017963-02/EY/NEI NIH HHS
Chemical
Reg. No./Substance:
0/Cyclin-Dependent Kinase Inhibitor p21; 0/Free Radical Scavengers; 0/Protein Subunits; 0/Reactive Oxygen Species; 0/Tumor Suppressor Protein p53; 616-91-1/Acetylcysteine; 70-18-8/Glutathione; EC 3.2.1.23/beta-Galactosidase; EC 6.3.2.2/Glutamate-Cysteine Ligase
Comments/Corrections

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


Previous Document:  Finding disease-specific coordinated functions by multi-function genes: Insight into the coordinatio...
Next Document:  Mitochondria and reactive oxygen species.