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Restoration of heat shock protein70 suppresses gastric mucosal inducible nitric oxide synthase expression induced by Helicobacter pylori
Author(s) -
Yeo Marie,
Park Hyunkyung,
Kim DongKyu,
Cho Sung Won,
Kim Young Suk,
Cho Sang Yun,
Paik Youngki,
Hahm KiBaik
Publication year - 2004
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.200400951
Subject(s) - cytoprotection , heat shock protein , helicobacter pylori , hsp70 , nitric oxide synthase , biology , gastric mucosa , inflammation , gastritis , apoptosis , immunology , nitric oxide , microbiology and biotechnology , stomach , biochemistry , gene , endocrinology , genetics
Abstract Heat shock proteins (HSPs) are crucial for the maintenance of cell integrity during normal cellular growth as well as during pathophysiological conditions. While functioning mainly as molecular chaperones, HSPs also appear to be involved in diverse biological activities, such as apoptosis, carcinogenesis, and cytoprotection from cytotoxic damage. Infection with Helicobacter pylori causes inflammation in the gastric mucosa, leading to gastritis, gastric ulcers, duodenal ulcer disease, and even gastric cancer, but the role of HSPs in H. pylori ‐associated gastropathy is not known. Using two‐dimensional electrophoretic analysis, we have observed significant shifts in HSP profiles after H. pylori infection in RGM‐1 cells. We therefore evaluated the effect of treatments that induce HSPs on H. pylori ‐induced inducible nitric oxide synthase (iNOS) expression. We found that H. pylori infection significantly attenuated the expression of HSP70, whereas exposure of cells to noncytotoxic heat shock or geranylgeranylacetone restored HSP70 expression, as well as suppressing the expression of iNOS, a major cause of H. pylori ‐induced gastric tissue damage. Our results suggest that induction of HSP70 confers cytoprotection against H. pylori infection by inhibiting the expression of iNOS. In conclusion, these results provide important insights into the flux in HSPs profiles in response to H. pylori infection and highlight the cytoprotective role of HSP70 in H. pylori infection.