Expression of suppressors of cytokine signaling-3 in Helicobacter pylori-infected rat gastric mucosal RGM-1cells

被引：6

作者：

Cha, Boram

Kim, Kyung Hwan

Matsui, Hirofumi

Kim, Hyeyoung ^{[1
]}

机构：

[1] Yonsei Univ, Coll Human Ecol, Dept Food & Nutr, Brain Korea Project 21, Seoul 120749, South Korea

[2] Yonsei Univ, Coll Med, Dept Pharmacol, Brain Korea Project Med Sci, Seoul 120752, South Korea

[3] Yonsei Univ, Coll Med, Inst Gastroenterol, Brain Korea Project Med Sci, Seoul 120752, South Korea

[4] Univ Tsukuba, Inst Clin Med, Div Gastroenterol, Tsukuba, Ibaraki 3058575, Japan

来源：

SIGNAL TRANSDUCTION PATHWAYS, PT D: INFLAMMATORY SIGNALING PATHWAYS AND NEUROPATHOLOGY | 2007年 / 1096卷

关键词：

Helicobacter pylori; RGM-1; cells; SOCS-3;

D O I：

10.1196/annals.1397.066

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Our previous studies show that Helicobacter pylori (H. pylori) induces oxidative stress and the expression of proinflammatory cytokines in gastric epithelial cells. H. pylori induces the expression of molecular chaperones and proteins involved in protein-folding machinery as a defense mechanism against cellular stress. The suppressors of cytokine signaling (SOCS) are known as negative regulators of major immune signal pathways. The purpose of this article is to determine whether H. pylori in a Korean isolate (HP99) induces the expression of SOCS in rat gastric mucosal RGM-1 cells as a defense mechanism. As a result, HP99 induced SOCS-3 expression time-dependently in RGM-1 cells. SOCS-1 was not expressed while SOCS-2 expression was not changed by HP99 infection in RGM-1 cells. SOCS-3 might have a defensive role in H. pylori-infected gastric mucosal cells. Further study by manipulating SOCS-3 gene should be performed to investigate the physiological meaning of SOCS-3 induced by H. pylori in gastric mucosal cells.

引用

页码：24 / 28

页数：5

共 13 条

[1] Oxidative-stress-related proteome changes in Helicobacter pylori-infected human gastric mucosa [J].