NF-κB and Bcl-2 in Helicobacter pylori - Induced Apoptosis in Gastric Epithelial Cells

Sang Hui Chu, Joo Weon Lim, Kyung Hwan Kim, Hye Young Kim

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Helicobacter pylori (H. pylori) has been considered as an important pathogen of gastroduodenal inflammation and gastric carcinogenesis. However, the pathogenic mechanisms including H. pylori-induced apoptosis and subsequent molecular mechanisms have not been clarified yet. The present study examined the role of Bcl-2 and its relation to NF-κB in H. pylori-induced apoptosis in human gastric epithelial AGS cells. AGS cells were cultured in the presence of H. pylori, at a bacterium/cell ratio of 300:1, for the determination of apoptosis, NF-κB activation with IκBα degradation, and Bcl-2 level. AGS cells were transfected with a control vector (pCMV cells) or a full-length human Bcl-2 expression vector (Bcl-2 cells). H. pylori-induced apoptosis and NF-κB activation were compared in the wild-type cells and the transfected cells. As a result, H. pylori increased apoptotic cells with chromatin condensation and reduced Bcl-2 levels, which were accompanied with NF-κB activation. H. pylori induced sixfold increase in the number of apoptotic cells in wild-type cells and pCMV cells. H. pylori-induced increment of apoptotic cells were relatively lower in Bcl-2 cells than pCMV cells. H. pylori-induced NF-κB activation and IκBα degradation were not different in the wild-type cells, pCMV cells, and Bcl-2 cells. In conclusion, the reduced gastric Bcl-2 level may be the main pathogenic mechanism of H. pylori-induced apoptosis in gastric epithelial cells.

Original languageEnglish
Pages (from-to)568-572
Number of pages5
JournalAnnals of the New York Academy of Sciences
Volume1010
DOIs
Publication statusPublished - 2003 Jan 1

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Helicobacter pylori
Stomach
Epithelial Cells
Apoptosis
Chemical activation
Cells
Degradation
Pathogens
Chromatin
Condensation
Bacteria
Cultured Cells
Carcinogenesis
Cell Count

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 = "NF-κB and Bcl-2 in Helicobacter pylori - Induced Apoptosis in Gastric Epithelial Cells",
abstract = "Helicobacter pylori (H. pylori) has been considered as an important pathogen of gastroduodenal inflammation and gastric carcinogenesis. However, the pathogenic mechanisms including H. pylori-induced apoptosis and subsequent molecular mechanisms have not been clarified yet. The present study examined the role of Bcl-2 and its relation to NF-κB in H. pylori-induced apoptosis in human gastric epithelial AGS cells. AGS cells were cultured in the presence of H. pylori, at a bacterium/cell ratio of 300:1, for the determination of apoptosis, NF-κB activation with IκBα degradation, and Bcl-2 level. AGS cells were transfected with a control vector (pCMV cells) or a full-length human Bcl-2 expression vector (Bcl-2 cells). H. pylori-induced apoptosis and NF-κB activation were compared in the wild-type cells and the transfected cells. As a result, H. pylori increased apoptotic cells with chromatin condensation and reduced Bcl-2 levels, which were accompanied with NF-κB activation. H. pylori induced sixfold increase in the number of apoptotic cells in wild-type cells and pCMV cells. H. pylori-induced increment of apoptotic cells were relatively lower in Bcl-2 cells than pCMV cells. H. pylori-induced NF-κB activation and IκBα degradation were not different in the wild-type cells, pCMV cells, and Bcl-2 cells. In conclusion, the reduced gastric Bcl-2 level may be the main pathogenic mechanism of H. pylori-induced apoptosis in gastric epithelial cells.",
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NF-κB and Bcl-2 in Helicobacter pylori - Induced Apoptosis in Gastric Epithelial Cells. / Chu, Sang Hui; Lim, Joo Weon; Kim, Kyung Hwan; Kim, Hye Young.

In: Annals of the New York Academy of Sciences, Vol. 1010, 01.01.2003, p. 568-572.

Research output: Contribution to journalArticle

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AB - Helicobacter pylori (H. pylori) has been considered as an important pathogen of gastroduodenal inflammation and gastric carcinogenesis. However, the pathogenic mechanisms including H. pylori-induced apoptosis and subsequent molecular mechanisms have not been clarified yet. The present study examined the role of Bcl-2 and its relation to NF-κB in H. pylori-induced apoptosis in human gastric epithelial AGS cells. AGS cells were cultured in the presence of H. pylori, at a bacterium/cell ratio of 300:1, for the determination of apoptosis, NF-κB activation with IκBα degradation, and Bcl-2 level. AGS cells were transfected with a control vector (pCMV cells) or a full-length human Bcl-2 expression vector (Bcl-2 cells). H. pylori-induced apoptosis and NF-κB activation were compared in the wild-type cells and the transfected cells. As a result, H. pylori increased apoptotic cells with chromatin condensation and reduced Bcl-2 levels, which were accompanied with NF-κB activation. H. pylori induced sixfold increase in the number of apoptotic cells in wild-type cells and pCMV cells. H. pylori-induced increment of apoptotic cells were relatively lower in Bcl-2 cells than pCMV cells. H. pylori-induced NF-κB activation and IκBα degradation were not different in the wild-type cells, pCMV cells, and Bcl-2 cells. In conclusion, the reduced gastric Bcl-2 level may be the main pathogenic mechanism of H. pylori-induced apoptosis in gastric epithelial cells.

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