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The Effect of p38 Mitogen‐Activated Protein Kinase on Mucin Gene Expression and Apoptosis in Helicobacter pylori ‐Infected Gastric Epithelial Cells
Author(s) -
KIM HYEYOUNG,
SEO JI HYE,
KIM KYUNG HWAN
Publication year - 2003
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1299.014
Subject(s) - mucin , apoptosis , helicobacter pylori , p38 mitogen activated protein kinases , mapk/erk pathway , microbiology and biotechnology , protein kinase a , biology , kinase , chemistry , cancer research , biochemistry , genetics
A bstract : The loss of mucus coat continuity and apoptosis have been shown in Helicobacter pylori ( H. pylori )‐infected gastric tissues. Blockade of p38 mitogen‐activated kinase (MAPK) produced reversal in the LPS‐induced reduction in mucin synthesis and apoptosis in gastric epithelial cells. This study investigates whether H. pylori induces apoptosis, alterations in mucin gene (MUC) expression, and p38 MAPK activation in human gastric epithelial AGS cells. After treatment of AGS cells with H. pylori at the ratio of 1:300, apoptosis was determined by DNA fragmentation and DNA laddering. MUC expression was assessed by RT‐PCR. p38 MAPK activation and mucin protein level, using anti‐mucin antibody for MUC5/6, were determined by Western blot analysis. As a result, H. pylori induced apoptosis and loss of mucin, which was supported by reduced mRNA expression of MUC5AC by H. pylori in AGS cells. MUC7/8 expression and p38 MAPK activation were induced in H. pylori ‐infected AGS cells. In conclusion, H. pylori induces p38 MAPK activation, wh3.ich may be the underlying mechanism of alterations in MUC expression and apoptosis in gastric epithelial cells.