Down-regulation of Bcl-2 is mediated by NF-kappa B activation in Helicobacter pylori-induced apoptosis of gastric epithelial cells

Title
Down-regulation of Bcl-2 is mediated by NF-kappa B activation in Helicobacter pylori-induced apoptosis of gastric epithelial cells
Author(s)
주상희[주상희]임주원[임주원]김동구[김동구]이응석김경환[김경환]김혜영[김혜영]
Keywords
ENDOTHELIAL APOPTOSIS; SIGNALING PATHWAY; ALPHA PROTEOLYSIS; IL-8 PRODUCTION; EXPRESSION; INFECTION; BAX; FAMILY; PHOSPHORYLATION; TRANSCRIPTION
Issue Date
201102
Publisher
INFORMA HEALTHCARE
Citation
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, v.46, no.2, pp.148 - 155
Abstract
Objective. Bcl-2 family is involved in the regulation of apoptosis. NF-kappa B activation is associated with either the expression of Bcl-2 or down-regulation of Bcl-2 depending on cell types and stimuli. Previously, we showed NF-kappa B activation, decrease in the level of Bcl-2, and apoptosis in Helicobacter pylori (H. pylori)-infected gastric epithelial cells. The present study aims to investigate the relation of Bcl-2 expression and NF-kappa B activation in H. pylori-induced apoptotic cell death of AGS (gastric adenocarcinoma) cells. Material and methods. AGS cells were transfected with mutant I kappa B alpha to suppress NF-kappa B activation or Bcl-2 gene to induce overexpression of Bcl-2. mRNA expression of Bcl-2, p53 and Bax, DNA fragmentation, cell viability, and the numbers of apoptotic cells were determined. Results. H. pylori induced decrease in Bcl-2, but increase in p53 and Bax at the levels of mRNA and protein in AGS cells. H. pylori-induced increment of apoptotic cells and decrease in Bcl-2 level were inhibited in the cells transfected with mutant I kappa B alpha gene as compared with the cells transfected with control vector. H. pylori-induced apoptosis determined by apoptotic cells, DNA fragmentation, and cell viability was inhibited in the cells transfected with Bcl-2 gene. Conclusion. Down-regulation of Bcl-2 is mediated by NF-kappa B activation, which may be the underlying mechanism of apoptosis in H. pylori-infected gastric epithelial cells.
URI
http://hdl.handle.net/YU.REPOSITORY/25691http://dx.doi.org/10.3109/00365521.2010.525255
ISSN
0036-5521
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약학대학 > 약학부 > Articles
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