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  Identification of novel Cyclooxygenase-2-dependent genes in Helicobacter pylori infection in vivo

Walduck, A., Weber, M., Wunder, C., Juettner, S., Stolte, M., Vieth, M., et al. (2009). Identification of novel Cyclooxygenase-2-dependent genes in Helicobacter pylori infection in vivo. Molecular Cancer, 8: 22.

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© 2009 Walduck et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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 Creators:
Walduck, Anna1, Author              
Weber, Matthias1, Author              
Wunder, Christian1, Author              
Juettner, Stefan1, Author              
Stolte, Manfred, Author
Vieth, Michael, Author
Wiedenmann, Bertram, Author
Meyer, Thomas F.1, Author              
Naumann, Michael1, Author              
Hoecker, Michael1, Author              
Affiliations:
1Department of Molecular Biology, Max Planck Institute for Infection Biology, Max Planck Society, ou_1664147              

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Free keywords: GASTRIC EPITHELIAL-CELLS; NONSTEROIDAL ANTIINFLAMMATORY DRUGS;; ORNITHINE-DECARBOXYLASE; IMMUNE-RESPONSES; COX-2 INHIBITION; IV; SECRETION; EXPRESSION; CANCER; PROTEIN; CARCINOMA
 Abstract: Background: Helicobacter pylori is a crucial determining factor in the pathogenesis of benign and neoplastic gastric diseases. Cyclooxygenase-2 (Cox-2) is the inducible key enzyme of arachidonic acid metabolism and is a central mediator in inflammation and cancer. Expression of the Cox-2 gene is up-regulated in the gastric mucosa during H. pylori infection but the pathobiological consequences of this enhanced Cox-2 expression are not yet characterized. The aim of this study was to identify novel genes down-stream of Cox-2 in an in vivo model, thereby identifying potential targets for the study of the role of Cox-2 in H. pylori pathogenesis and the initiation of pre-cancerous changes. Results: Gene expression profiles in the gastric mucosa of mice treated with a specific Cox-2 inhibitor (NS398) or vehicle were analysed at different time points (6, 13 and 19 wk) after H. pylori infection. H. pylori infection affected the expression of 385 genes over the experimental period, including regulators of gastric physiology, proliferation, apoptosis and mucosal defence. Under conditions of Cox-2 inhibition, 160 target genes were regulated as a result of H. pylori infection. The Cox-2 dependent subset included those influencing gastric physiology (Gastrin, Galr1), epithelial barrier function (Tjp1, connexin45, Aqp5), inflammation (Icam1), apoptosis (Clu) and proliferation (Gdf3, Igf2). Treatment with NS398 alone caused differential expression of 140 genes, 97 of which were unique, indicating that these genes are regulated under conditions of basal Cox-2 expression. Conclusion: This study has identified a panel of novel Cox-2 dependent genes influenced under both normal and the inflammatory conditions induced by H. pylori infection. These data provide important new links between Cox-2 and inflammatory processes, epithelial repair and integrity.

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Language(s): eng - English
 Dates: 2009-03
 Publication Status: Published in print
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 Rev. Type: -
 Identifiers: eDoc: 439950
ISI: 000265255900001
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Title: Molecular Cancer
Source Genre: Journal
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Pages: - Volume / Issue: 8 Sequence Number: 22 Start / End Page: - Identifier: ISSN: 1476-4598 %R 22 10.1186/1476-4598-8-22