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Analysis of Gene Expression Profile of AGS Cells Stimulated by Helicobacter pylori Adhesionopen access

Authors
Kim, NayoungPark, Woong YangKim, Jung MoggPark, Young SooLee, Dong HoPark, Ji HyunKim, Joo SungJung, Hyun ChaeSong, In Sung
Issue Date
Jun-2007
Publisher
EDITORIAL OFFICE GUT & LIVER
Keywords
Helicobacter pylori; Host cell; Adhesion; Microarray
Citation
GUT AND LIVER, v.1, no.1, pp.40 - 48
Indexed
SCIE
Journal Title
GUT AND LIVER
Volume
1
Number
1
Start Page
40
End Page
48
URI
https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/180061
DOI
10.5009/gnl.2007.1.1.40
ISSN
1976-2283
Abstract
Background/Aims: Interactions between H. pylori and gastric epithelial cells contribute to gastric inflammation and epithelial damage. This study was performed to evaluate the gene expression profile of AGS cells by adhesion of H. pylori. Methods: 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. Realtime 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, DD132, 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. (Gut and Liver 2007;1:40-48)
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