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HSP90beta interacts with Rac1 to activate NADPH oxidase in Helicobacter pylori-infected gastric epithelial cells

Authors
 Soon Ok Cho  ;  Joo Weon Lim  ;  Jong-Ho Jun  ;  Kyung Hwan Kim  ;  Hyeyoung Kim 
Citation
 INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, Vol.42(9) : 1455-1461, 2010 
Journal Title
 INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY 
ISSN
 1357-2725 
Issue Date
2010
MeSH
Blotting, Western ; Cell Line ; Cytosol/metabolism ; Epithelial Cells/metabolism* ; Epithelial Cells/microbiology* ; Gastric Mucosa/cytology ; HSP90 Heat-Shock Proteins/genetics ; HSP90 Heat-Shock Proteins/metabolism* ; Helicobacter Infections/microbiology ; Helicobacter Infections/physiopathology* ; Helicobacter pylori/physiology* ; Humans ; Immunoprecipitation ; NADPH Oxidases/genetics ; NADPH Oxidases/metabolism* ; Protein Transport ; RNA, Small Interfering ; rac1 GTP-Binding Protein/genetics ; rac1 GTP-Binding Protein/metabolism*
Keywords
Helicobacter pylori ; HSP90β ; Rac1 ; NADPH oxidase ; AGS cells
Abstract
Reactive oxygen species (ROS) are involved in the pathogenesis of Helicobacter pylori (H. pylori)-induced gastric disorders including inflammation. NADPH oxidase has been considered as a major source of ROS in phagocytic and non-phagocytic cells. Small G protein Rac1 is one components of NADPH oxidase complex. Heat shock protein 90 kDa (HSP90) modulates cytokine production in H. pylori-infected gastric epithelial cells. The present study aims to investigate the relation of HSP90beta and Rac1 on the activation of NADPH oxidase in H. pylori-infected gastric epithelial cells. As a result, H. pylori-induced translocation of HSP90beta from the cytosol to the membrane and activated Rac1 in gastric epithelial AGS cells. HSP90beta physically interacted with Rac1, which resulted in the activation of NADPH oxidase in H. pylori-infected AGS cells. Down-regulation of HSP90beta by transfection of HSP90beta siRNA suppressed the activation of Rac1, activity of NADPH oxidase and the production of H(2)O(2) in H. pylori-infected AGS cells. In conclusion, H. pylori induces the translocation of HSP90beta from the cytosol to the membrane and interaction of HSP90beta and Rac1, which leads to the activation of NADPH oxidase and production of ROS in gastric epithelial cells. HSP90beta may be the target molecule for treatment of H. pylori-induced gastric injury.
Full Text
http://www.sciencedirect.com/science/article/pii/S1357272510001664
DOI
10.1016/j.biocel.2010.04.015
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers
Yonsei Authors
Kim, Kyung Hwan(김경환)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/101316
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