The Effect of p38 Mitogen-Activated Protein Kinase on Mucin Gene Expression and Apoptosis in Helicobacter pylori-Infected Gastric Epithelial Cells

Hye Young Kim, Ji Hye Seo, Kyung Hwan Kim

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Abstract

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 antimucin 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.

Original languageEnglish
Pages (from-to)90-94
Number of pages5
JournalAnnals of the New York Academy of Sciences
Volume1010
DOIs
Publication statusPublished - 2003 Jan 1

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p38 Mitogen-Activated Protein Kinases
Mucins
Gene expression
Helicobacter pylori
Stomach
Epithelial Cells
Apoptosis
Gene Expression
Chemical activation
DNA
Mitogen-Activated Protein Kinase Kinases
Mitogens
DNA Fragmentation
Mucus
Protein
Cells
Tissue
Western Blotting
Messenger RNA
Activation

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

Cite this

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title = "The Effect of p38 Mitogen-Activated Protein Kinase on Mucin Gene Expression and Apoptosis in Helicobacter pylori-Infected Gastric Epithelial Cells",
abstract = "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 antimucin 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.",
author = "Kim, {Hye Young} and Seo, {Ji Hye} and Kim, {Kyung Hwan}",
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AU - Seo, Ji Hye

AU - Kim, Kyung Hwan

PY - 2003/1/1

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N2 - 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 antimucin 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.

AB - 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 antimucin 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.

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