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 language | English |
|---|---|
| Pages (from-to) | 568-572 |
| Number of pages | 5 |
| Journal | Annals of the New York Academy of Sciences |
| Volume | 1010 |
| DOIs | |
| Publication status | Published - 2003 Jan 1 |
Fingerprint
All Science Journal Classification (ASJC) codes
- Neuroscience(all)
- Biochemistry, Genetics and Molecular Biology(all)
- History and Philosophy of Science
Cite this
}
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 journal › Article
TY - JOUR
T1 - NF-κB and Bcl-2 in Helicobacter pylori - Induced Apoptosis in Gastric Epithelial Cells
AU - Chu, Sang Hui
AU - Lim, Joo Weon
AU - Kim, Kyung Hwan
AU - Kim, Hye Young
PY - 2003/1/1
Y1 - 2003/1/1
N2 - 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.
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.
UR - http://www.scopus.com/inward/record.url?scp=1342284256&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=1342284256&partnerID=8YFLogxK
U2 - 10.1196/annals.1299.106
DO - 10.1196/annals.1299.106
M3 - Article
C2 - 15033793
AN - SCOPUS:1342284256
VL - 1010
SP - 568
EP - 572
JO - Annals of the New York Academy of Sciences
JF - Annals of the New York Academy of Sciences
SN - 0077-8923
ER -