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KMID : 1188320070010010040
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Gut and Liver
2007 Volume.1 No. 1 p.40 ~ p.48
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Analysis of Gene Expression Profile of AGS Cells Stimulated by Helicobacter pylori Adhesion
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Kim Na-Young
Park Woong-Yang
Kim Jung-Mogg
Park Young-Soo
Lee Dong-Ho
Park Ji-Hyun
Kim Joo-Sung
Jung Hyun-Chae
Song In-Sung
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Abstract
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Background:Interactions between H. pylori and gastric epithelial cells contribute to gastric inflam-mation and epithelial damage. This study was performed to evaluate the gene expression profile of AGS cells by adhesion of H. pylori.
Method:Changes in AGS cell gene expression induced by co-culturing with H. pylori (G69a strain) (4, 12, 24, 48 hours) were monitored using oligonucleotide microarray. Real- time reverse transcription-polymerase chain reaction (RT-PCR) was performed for data validation by the Assay-on-Demand Gene Expression product method.
Results:A total of 270 (2.66%) and 19 genes (0.19%) were up-regulated in AGS cells by H. pylori adhesion. Gene ontology analysis showed that up-regulated genes were categorized into endolipidase activity (17 genes), receptor binding (17 genes), integrin binding (4 genes), and two down-regulated genes into GTP binding category. The expression levels of 20 up- and 5 down-regulated genes were quantified by real-time RT-PCR. Sixteen genes involving cytokine activity (IL8, IL1B, TNF), hydrolase activity (PTP4A1, ERCC1, CASP8, CASP7, ACIN1), VIP receptor activity (VIPR2), and neuropeptide Y receptor activity (GPR83) were confirmed to be up-regulated. Five genes, namely, ARF3, M17S2, DDB2, AWP1, and WTAP were confirmed to be down-regulated.
Conclusions: Host genes are significantly changed by H. pylori adhesion, which might explain the gastroduodenal pathogenesis induced by H. pylori infection.
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KEYWORD
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Helicobacter pylori, Host cell, Adhesion, Microarray
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