Document Detail


Spermine oxidation induced by Helicobacter pylori results in apoptosis and DNA damage: implications for gastric carcinogenesis.
MedLine Citation:
PMID:  15574757     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Oxidative stress is linked to carcinogenesis due to its ability to damage DNA. The human gastric pathogen Helicobacter pylori exerts much of its pathogenicity by inducing apoptosis and DNA damage in host gastric epithelial cells. Polyamines are abundant in epithelial cells, and when oxidized by the inducible spermine oxidase SMO(PAOh1) H(2)O(2) is generated. Here, we report that H. pylori up-regulates mRNA expression, promoter activity, and enzyme activity of SMO(PAOh1) in human gastric epithelial cells, resulting in DNA damage and apoptosis. H. pylori-induced H(2)O(2) generation and apoptosis in these cells was equally attenuated by an inhibitor of SMO(PAOh1), by catalase, and by transient transfection with small interfering RNA targeting SMO(PAOh1). Conversely, SMO(PAOh1) overexpression induced apoptosis to the same levels as caused by H. pylori. Importantly, in H. pylori-infected tissues, there was increased expression of SMO(PAOh1) in both human and mouse gastritis. Laser capture microdissection of human gastric epithelial cells demonstrated expression of SMO(PAOh1) that was significantly attenuated by H. pylori eradication. These results identify a pathway for oxidative stress-induced epithelial cell apoptosis and DNA damage due to SMO(PAOh1) activation by H. pylori that may contribute to the pathogenesis of the infection and development of gastric cancer.
Authors:
Hangxiu Xu; Rupesh Chaturvedi; Yulan Cheng; Francoise I Bussiere; Mohammad Asim; Micheal D Yao; Darryn Potosky; Stephen J Meltzer; Juong G Rhee; Sung S Kim; Steven F Moss; Amy Hacker; Yanlin Wang; Robert A Casero; Keith T Wilson
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Cancer research     Volume:  64     ISSN:  0008-5472     ISO Abbreviation:  Cancer Res.     Publication Date:  2004 Dec 
Date Detail:
Created Date:  2004-12-02     Completed Date:  2005-01-27     Revised Date:  2011-11-02    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  8521-5     Citation Subset:  IM    
Affiliation:
Department of Medicine, Division of Gastroenterology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / physiology*
DNA Damage / physiology*
Enzyme Induction
Gastric Mucosa / enzymology,  metabolism*,  microbiology*
Gene Expression Regulation, Enzymologic
Gene Silencing
Helicobacter Infections / enzymology,  metabolism*
Helicobacter pylori / metabolism*
Humans
Hydrogen Peroxide / metabolism
Oxidation-Reduction
Oxidative Stress
Oxidoreductases Acting on CH-NH Group Donors / biosynthesis,  genetics,  metabolism
Promoter Regions, Genetic
RNA, Messenger / biosynthesis,  genetics
Spermine / metabolism*
Stomach / enzymology,  metabolism,  microbiology
Stomach Neoplasms / enzymology,  metabolism,  microbiology*
Grant Support
ID/Acronym/Agency:
CA01808/CA/NCI NIH HHS; CA51085/CA/NCI NIH HHS; CA77057/CA/NCI NIH HHS; CA85069/CA/NCI NIH HHS; CA95323/CA/NCI NIH HHS; CA98454/CA/NCI NIH HHS; DK53620/DK/NIDDK NIH HHS; DK63626/DK/NIDDK NIH HHS; RR17695/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/RNA, Messenger; 71-44-3/Spermine; 7722-84-1/Hydrogen Peroxide; EC 1.5.-/Oxidoreductases Acting on CH-NH Group Donors; EC 1.5.3.-/polyamine oxidase

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