Document Detail


p53 controls radiation-induced gastrointestinal syndrome in mice independent of apoptosis.
MedLine Citation:
PMID:  20019247     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Acute exposure to ionizing radiation can cause lethal damage to the gastrointestinal (GI) tract, a condition called the GI syndrome. Whether the target cells affected by radiation to cause the GI syndrome are derived from the epithelium or endothelium and whether the target cells die by apoptosis or other mechanisms are controversial issues. Studying mouse models, we found that selective deletion of the proapoptotic genes Bak1 and Bax from the GI epithelium or from endothelial cells did not protect mice from developing the GI syndrome after sub-total-body gamma irradiation. In contrast, selective deletion of p53 from the GI epithelium, but not from endothelial cells, sensitized irradiated mice to the GI syndrome. Transgenic mice overexpressing p53 in all tissues were protected from the GI syndrome after irradiation. These results suggest that the GI syndrome is caused by the death of GI epithelial cells and that these epithelial cells die by a mechanism that is regulated by p53 but independent of apoptosis.
Authors:
David G Kirsch; Philip M Santiago; Emmanuelle di Tomaso; Julie M Sullivan; Wu-Shiun Hou; Talya Dayton; Laura B Jeffords; Pooja Sodha; Kim L Mercer; Rhianna Cohen; Osamu Takeuchi; Stanley J Korsmeyer; Roderick T Bronson; Carla F Kim; Kevin M Haigis; Rakesh K Jain; Tyler Jacks
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-12-17
Journal Detail:
Title:  Science (New York, N.Y.)     Volume:  327     ISSN:  1095-9203     ISO Abbreviation:  Science     Publication Date:  2010 Jan 
Date Detail:
Created Date:  2010-01-29     Completed Date:  2010-02-17     Revised Date:  2011-11-28    
Medline Journal Info:
Nlm Unique ID:  0404511     Medline TA:  Science     Country:  United States    
Other Details:
Languages:  eng     Pagination:  593-6     Citation Subset:  IM    
Affiliation:
David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis*
Cell Death
Epithelial Cells / cytology,  physiology,  radiation effects
Gamma Rays / adverse effects*
Gene Deletion
Genes, p53
Intestinal Diseases / etiology,  pathology,  physiopathology*
Intestinal Mucosa / pathology,  physiopathology,  radiation effects*
Intestine, Small / pathology,  physiopathology,  radiation effects*
Mesoderm / cytology
Mice
Mice, Transgenic
Models, Biological
Radiation Dosage
Radiation Injuries / etiology,  pathology,  physiopathology*
Tumor Suppressor Protein p53 / physiology*
bcl-2 Homologous Antagonist-Killer Protein / genetics,  metabolism
bcl-2-Associated X Protein / genetics,  metabolism
Grant Support
ID/Acronym/Agency:
K08 CA 114176/CA/NCI NIH HHS; K08 CA114176-05/CA/NCI NIH HHS; P01 CA080124-01A1/CA/NCI NIH HHS; P01 CA80124/CA/NCI NIH HHS; P30 CA014051-38/CA/NCI NIH HHS; P30-CA14051/CA/NCI NIH HHS; RC1 AI078521-01/AI/NIAID NIH HHS; RC1-AI078521/AI/NIAID NIH HHS; U19-AI06775/AI/NIAID NIH HHS; //Howard Hughes Medical Institute; //Howard Hughes Medical Institute
Chemical
Reg. No./Substance:
0/Bak1 protein, mouse; 0/Bax protein, mouse; 0/Tumor Suppressor Protein p53; 0/bcl-2 Homologous Antagonist-Killer Protein; 0/bcl-2-Associated X Protein
Comments/Corrections
Erratum In:
Science. 2011 Nov 11;334(6057):761

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