Document Detail


Dual regulation by apurinic/apyrimidinic endonuclease-1 inhibits gastric epithelial cell apoptosis during Helicobacter pylori infection.
MedLine Citation:
PMID:  20332233     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Human apurinic/apyrimidinic endonuclease-1 (APE-1), a key enzyme involved in repair of oxidative DNA base damage, is an important transcriptional coregulator. We previously reported that Helicobacter pylori infection induces apoptosis and increases APE-1 expression in human gastric epithelial cells (GEC). Although both the DNA repair activity and the acetylation-mediated transcriptional regulation of APE-1 are required to prevent cell death, the mechanisms of APE-1-mediated inhibition of infection-induced apoptosis are unclear. Here, we show that short hairpin RNA-mediated stable suppression of APE-1 results in increased apoptosis in GEC after H. pylori infection. We show that programmed cell death involves both the caspase-9-mediated mitochondrial pathway and the caspase-8-dependent extrinsic pathway by measuring different markers for both the pathways. Overexpression of wild-type APE-1 in APE-1-suppressed GEC reduced apoptosis after infection; however, overexpression of the DNA repair mutant or the nonacetylable mutant of APE-1 alone was unable to reduce apoptosis, suggesting that both DNA repair and acetylation functions of APE-1 modulate programmed cell death. We show for the first time that the DNA repair activity of APE-1 inhibits the mitochondrial pathway, whereas the acetylation function inhibits the extrinsic pathway during H. pylori infection. Thus, our findings establish that the two different functions of APE-1 differentially regulate the intrinsic and the extrinsic pathway of H. pylori-mediated GEC apoptosis. As proapoptotic and antiapoptotic mechanisms determine the development and progression of gastritis, gastric ulceration, and gastric cancer, this dual regulatory role of APE-1 represents one of the important molecular strategies by H. pylori to sustain chronic infection.
Authors:
Ranajoy Chattopadhyay; Asima Bhattacharyya; Sheila E Crowe
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-03-23
Journal Detail:
Title:  Cancer research     Volume:  70     ISSN:  1538-7445     ISO Abbreviation:  Cancer Res.     Publication Date:  2010 Apr 
Date Detail:
Created Date:  2010-04-02     Completed Date:  2010-05-03     Revised Date:  2011-08-01    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2799-808     Citation Subset:  IM    
Affiliation:
Department of Medicine, University of Virginia, Charlottesville, VA 22908-0708, USA.
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MeSH Terms
Descriptor/Qualifier:
Acetylation
Adenocarcinoma / enzymology*,  genetics,  microbiology,  pathology
Apoptosis / physiology*
Cell Line, Tumor
DNA Repair
DNA-(Apurinic or Apyrimidinic Site) Lyase / genetics,  metabolism*
Helicobacter Infections / enzymology*,  genetics,  pathology
Helicobacter pylori / physiology*
Humans
Mitochondria / physiology
Stomach Neoplasms / enzymology*,  genetics,  microbiology,  pathology
Transfection
Grant Support
ID/Acronym/Agency:
R01 DK061769-07/DK/NIDDK NIH HHS; R01 DK061769-07S1/DK/NIDDK NIH HHS; R01 DK61769/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
EC 4.2.99.18/APEX1 protein, human; EC 4.2.99.18/DNA-(Apurinic or Apyrimidinic Site) Lyase
Comments/Corrections

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