Abstract
In Helicobacter pylori (H. pylori)-induced gastric ulceration, NF-κB regulates the expression of inflammatory genes. NF-κB is activated by phsophorylation of its endogenous inhibitor, IκBα. The possible involvement of mitogenactivated protein kinase (MAPK) on NF-κB activation has been suggested in various cells. Present study aims to investigate whether H. pylori in a Korean isolate induces phosphorylation of IkBα and whether H. pylori-induced phosphorylation of IkBα is mediated by MAPK in gastric epithelial AGS cells. AGS cells were treated with MAPK inhibitors (U0126 for extracellular signal-regulated kinase, SB203580 for p38 kinase, SP600125 for c-Jun NH2-terminal protein kinases) and stimulated with H. pylori. As a result, H. pylori increased phospho-specific IκBα accompanied with the decrease in control IκBα. H. pylori-induced phosphorylation of IκBα was inhibited by treatment of U0126, but not by SB203580 or SP600125. In conclusion, extracellular signal-regulated kinase induces phosphorylation of IκBα in H. pylori-infected AGS cells.
| Original language | English |
|---|---|
| Pages (from-to) | 26-30 |
| Number of pages | 5 |
| Journal | Inflammopharmacology |
| Volume | 15 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2007 Feb 1 |
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All Science Journal Classification (ASJC) codes
- Immunology
- Pharmacology
- Pharmacology (medical)
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Extracellular signal-regulated kinase induces phosphorylation of IκBα in Helicobacter pylori-infected gastric epithelial AGS cells. / Cho, S. O.; Kim, K. H.; Kim, H.
In: Inflammopharmacology, Vol. 15, No. 1, 01.02.2007, p. 26-30.Research output: Contribution to journal › Article
TY - JOUR
T1 - Extracellular signal-regulated kinase induces phosphorylation of IκBα in Helicobacter pylori-infected gastric epithelial AGS cells
AU - Cho, S. O.
AU - Kim, K. H.
AU - Kim, H.
PY - 2007/2/1
Y1 - 2007/2/1
N2 - In Helicobacter pylori (H. pylori)-induced gastric ulceration, NF-κB regulates the expression of inflammatory genes. NF-κB is activated by phsophorylation of its endogenous inhibitor, IκBα. The possible involvement of mitogenactivated protein kinase (MAPK) on NF-κB activation has been suggested in various cells. Present study aims to investigate whether H. pylori in a Korean isolate induces phosphorylation of IkBα and whether H. pylori-induced phosphorylation of IkBα is mediated by MAPK in gastric epithelial AGS cells. AGS cells were treated with MAPK inhibitors (U0126 for extracellular signal-regulated kinase, SB203580 for p38 kinase, SP600125 for c-Jun NH2-terminal protein kinases) and stimulated with H. pylori. As a result, H. pylori increased phospho-specific IκBα accompanied with the decrease in control IκBα. H. pylori-induced phosphorylation of IκBα was inhibited by treatment of U0126, but not by SB203580 or SP600125. In conclusion, extracellular signal-regulated kinase induces phosphorylation of IκBα in H. pylori-infected AGS cells.
AB - In Helicobacter pylori (H. pylori)-induced gastric ulceration, NF-κB regulates the expression of inflammatory genes. NF-κB is activated by phsophorylation of its endogenous inhibitor, IκBα. The possible involvement of mitogenactivated protein kinase (MAPK) on NF-κB activation has been suggested in various cells. Present study aims to investigate whether H. pylori in a Korean isolate induces phosphorylation of IkBα and whether H. pylori-induced phosphorylation of IkBα is mediated by MAPK in gastric epithelial AGS cells. AGS cells were treated with MAPK inhibitors (U0126 for extracellular signal-regulated kinase, SB203580 for p38 kinase, SP600125 for c-Jun NH2-terminal protein kinases) and stimulated with H. pylori. As a result, H. pylori increased phospho-specific IκBα accompanied with the decrease in control IκBα. H. pylori-induced phosphorylation of IκBα was inhibited by treatment of U0126, but not by SB203580 or SP600125. In conclusion, extracellular signal-regulated kinase induces phosphorylation of IκBα in H. pylori-infected AGS cells.
UR - http://www.scopus.com/inward/record.url?scp=33847339863&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33847339863&partnerID=8YFLogxK
U2 - 10.1007/s10787-006-1547-z
DO - 10.1007/s10787-006-1547-z
M3 - Article
C2 - 17323192
AN - SCOPUS:33847339863
VL - 15
SP - 26
EP - 30
JO - Inflammopharmacology
JF - Inflammopharmacology
SN - 0925-4692
IS - 1
ER -