首页> 外文会议>Meeting on Cell Signaling World >Expression of Suppressors of Cytokine Signaling-3 in Helicobacter pylori-Infected Rat Gastric Mucosal RGM-1 Cells
【24h】

Expression of Suppressors of Cytokine Signaling-3 in Helicobacter pylori-Infected Rat Gastric Mucosal RGM-1 Cells

机译:细胞因子信号-3在幽门螺杆菌感染大鼠胃黏膜RGM-1细胞中抑制剂的表达

获取原文

摘要

Our previous studies show that Helicobacter pylori (H. pylori) induces oxidative stress and the expression of proinflamma tory cytokines in gastric epithelial cells. H. pylori induces the expression of molecular chaperones and proteins involved in protein-folding ma chinery as a defense mechanism against cellular stress. The suppressors of cytokine signaling (SOCS) are known as negative regulators of ma jor 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 de fensive role in H. pylori-infected gastric mucosal cells. Further study by manipulating SOCS-3 gene should be performed to investigate the phys iological meaning of SOCS-3 induced by H. pylori in gastric mucosal cells.
机译:我们以前的研究表明,幽门螺杆菌(H.Pylori)诱导氧化应激和胃上皮细胞中Prinflamma Tory细胞因子的表达。 H. Pylori诱导分子伴侣和蛋白质的表达,参与蛋白质折叠MA Chinery作为对细胞应激的防御机制。细胞因子信号传导(SoC)的抑制剂称为MA JOR免疫信号途径的负调节剂。本文的目的是确定韩国分离物(HP99)中的幽门螺杆菌是否诱导大鼠胃粘膜RGM-1细胞中SOC的表达作为防御机制。结果,HP99在RGM-1细胞中依赖于时间诱导SOCS-3表达。 SOCS-1未表达,而RGM-1细胞中HP99感染没有改变SOCS-2表达。 SOCS-3可能在H. Pylori感染的胃粘膜细胞中具有De冥想的作用。应进行操作,以进行操纵SOCS-3基因的进一步研究,以研究H. Pylori在胃粘膜细胞中诱导的SOCS-3的物理学意义。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号