TITLE

HELICOBACTER PYLORI REGULATES ID-1 AND ID-3 EXPRESSION, BUT NOT ID-2

AUTHOR(S)
Manzo, B.A.; Bajaj-Elliott, M.; Atherton, J.; Thomas, R.; Sanderson, I.R.; Wilson, J.W.
PUB. DATE
April 2003
SOURCE
Gut;Apr2003 Supplement 1, Vol. 52, pA8
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
H pylori can induce both apoptosis and proliferation of gastric epithelial cells. The balance between these two processes during bacterial infection depends on both host and microbial determinants and underlay the risk of developing cancer. Inhibitor of differentiation (Id/DNA binding) helix-loop-helix proteins are critically related to cell cycle progression, differentiation, and apoptosis. These effects are mediated by inhibiting the DNA binding of basic HLH transcription factors, such as the ubiquitous E47 and tissue-specific factors like myoD. We hypothesised that H pylori could regulate Id expression in gastric epithelial cells following infection. AGS cells (from a poorly differentiated gastric adenocarcinoma) were co-cuhured with H pylori 60190 wild type strain (1×108 bacteria/cell) from 2 to 48 hours. RT-PCR analysis revealed down-regulation for Id-1 and Id-3 mRNA levels, which occurred over the first 6 hours of exposure to H pylori. In contrast, Id-2 mRNA levels remained constant. In agreement with transcriptional data, Western blot analysis showed that protein levels were strongly and rapidly downregulated by the bacteria; again Id-2 protein levels were unaltered. Culture of AGS cells in presence of H pylori resulted in the accumulation of cells in the G1 phase of the cell cycle (69% after 24 hours compared with 48% in control cultures), as assessed by FACS analysis. No significant apoptosis was observed. In conclusion, H pylori results in decreased Id-1 and Id-3 expression in AGS cells in vitro, which is associated with arrest of the cells in G1 phase of the cell cycle. These results indicate that H pylori can alter the expression of key regulatory transcription factors controlling gene expression in the cell cycle.
ACCESSION #
9747305

 

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