Up-regulated smad5 mediates apoptosis of gastric epithelial cells induced by Helicobacter pylori infection

被引：31

作者：

Nagasako, T ^{[1
]}

Sugiyama, T ^{[1
]}

Mizushima, T ^{[1
]}

Miura, Y ^{[1
]}

Kato, M ^{[1
]}

Asaka, M ^{[1
]}

机构：

[1] Hokkaido Univ, Grad Sch Med, Dept Gastroenterol, Kita Ku, Sapporo, Hokkaido 0608638, Japan

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 2003年 / 278卷 / 07期

关键词：

D O I：

10.1074/jbc.M211143200

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The gastric pathogen Helicobacter pylori activates epithelial cell signaling pathways, and its infection induces changes in the expression of several genes in infected human gastric tissues. Recent studies have indicated that the ability of H. pylori to regulate epithelial cell responses depends on the presence of an intact cag pathogenicity island (cagPAI). We investigated altered mRNA expression of gastric epithelial cells after infection with H. pylori, both cagPAI-positive and cagPAI-negative strains, by cDNA microarray, reverse transcription PCR, and Northern blot analysis. Our results indicated that cagPAI-positive H. pylori strains (ATCC 43504 and clinical isolated strains) significantly activated Smad5 mRNA expression of human gastric epithelial cells (AGS, KATOIII, MKN28, and MEN45). We further examined whether the up-regulated Smad5 was related to apoptosis of gastric epithelial cells induced by H. pylori. Smad5 RNA interference completely inhibited H. pylori-induced apoptosis. These results suggest that Smad5 is up-regulated in gastric epithelial cells through the presence of cagPAI of H. pylori and that Smad5 mediates apoptosis of gastric epithelial cells induced by H. pylori infection.

引用

页码：4821 / 4825

页数：5

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