KMID : 1140220130180040346
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´ëÇѾϿ¹¹æÇÐȸÁö 2013 Volume.18 No. 4 p.346 ~ p.350
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Differential Role of ERK and p38 on NF-¥êB Activation in Helicobacter pylori-Infected Gastric Epithelial Cells
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Seo Ji-Hye
Lim Joo-Weon Kim Hye-Young
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Abstract
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Gastric cancer, as well as inflammation, caused by Helicobacter pylori, activates the production of chemokines by activation of redox-sensitive transcription factor NF-¥êB in gastric epithelial cells. Mitogen-activated protein kinases including extracellular signal-regulated kinase (ERK) and p38 kinase (p38) are activated by Helicobacter pylori, which may regulate NF-¥êB activation in the infected cells. However the mechanisms how ERK and p38 induce NF-¥êB activation have not been investigated. Present study aims to investigate the role of ERK and p38 on the activation of NF-¥êB in Helicobacter pylori-infected AGS cells. Western blot analysis was performed for determining the levels of I¥êB, p105, p50 and p65 in gastric epithelial cells infected with Helicobacter pylori and treated with ERK inhibitor U0126 and p38 inhibitor SB203580. Helicobacter pylori induced the degradation of I¥êB¥á and upregulation of p105, p50 and p65 in the infected cells. U0126 inhibited the degradation of I¥êB¥á while SB203580 suppressed expression of p105, p50 and p65 in Helicobacter pylori-infected cells. ERK and p38 differentially activate NF-¥êB; ERK induces degradation of I¥êB¥á while p38 upregulates the expression of p50 and p65, subunits of NF-¥êB in Helicobacter pylori-infected gastric epithelial AGS cells.
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KEYWORD
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ERK, p38, NF-¥êB, Helicobacter pylori
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