Document Detail


A human-like senescence-associated secretory phenotype is conserved in mouse cells dependent on physiological oxygen.
MedLine Citation:
PMID:  20169192     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cellular senescence irreversibly arrests cell proliferation in response to oncogenic stimuli. Human cells develop a senescence-associated secretory phenotype (SASP), which increases the secretion of cytokines and other factors that alter the behavior of neighboring cells. We show here that "senescent" mouse fibroblasts, which arrested growth after repeated passage under standard culture conditions (20% oxygen), do not express a human-like SASP, and differ from similarly cultured human cells in other respects. However, when cultured in physiological (3%) oxygen and induced to senesce by radiation, mouse cells more closely resemble human cells, including expression of a robust SASP. We describe two new aspects of the human and mouse SASPs. First, cells from both species upregulated the expression and secretion of several matrix metalloproteinases, which comprise a conserved genomic cluster. Second, for both species, the ability to promote the growth of premalignant epithelial cells was due primarily to the conserved SASP factor CXCL-1/KC/GRO-alpha. Further, mouse fibroblasts made senescent in 3%, but not 20%, oxygen promoted epithelial tumorigenesis in mouse xenographs. Our findings underscore critical mouse-human differences in oxygen sensitivity, identify conditions to use mouse cells to model human cellular senescence, and reveal novel conserved features of the SASP.
Authors:
Jean-Philippe Coppé; Christopher K Patil; Francis Rodier; Ana Krtolica; Christian M Beauséjour; Simona Parrinello; J Graeme Hodgson; Koei Chin; Pierre-Yves Desprez; Judith Campisi
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2010-02-12
Journal Detail:
Title:  PloS one     Volume:  5     ISSN:  1932-6203     ISO Abbreviation:  PLoS ONE     Publication Date:  2010  
Date Detail:
Created Date:  2010-02-19     Completed Date:  2010-09-30     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101285081     Medline TA:  PLoS One     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e9188     Citation Subset:  IM    
Affiliation:
Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California, United States of America.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blotting, Western
Cell Aging / genetics,  physiology*
Cells, Cultured
DNA Damage
Epithelial Cells / metabolism,  physiology,  secretion
Fibroblasts / metabolism,  physiology*,  secretion
Genomic Instability
Humans
Insulin-Like Growth Factor Binding Protein 6 / genetics,  metabolism
Interleukin-6 / genetics,  metabolism
Intracellular Signaling Peptides and Proteins / genetics,  metabolism
Matrix Metalloproteinases / genetics,  metabolism
Mice
Mice, Inbred C57BL
Mice, Nude
Neoplasms, Experimental / genetics,  metabolism,  pathology
Oxygen / metabolism,  physiology*
Phenotype
Proteome / genetics,  metabolism*
Proteomics / methods
Reverse Transcriptase Polymerase Chain Reaction
Species Specificity
Transplantation, Heterologous
Tumor Burden
Grant Support
ID/Acronym/Agency:
AG000266/AG/NIA NIH HHS; AG0025708/AG/NIA NIH HHS; AG017242/AG/NIA NIH HHS; AG09909/AG/NIA NIH HHS; CA126540/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Insulin-Like Growth Factor Binding Protein 6; 0/Interleukin-6; 0/Intracellular Signaling Peptides and Proteins; 0/Proteome; 0/Trp53bp1 protein, mouse; 7782-44-7/Oxygen; EC 3.4.24.-/Matrix Metalloproteinases
Comments/Corrections

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