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Erschienen in: Digestive Diseases and Sciences 3/2007

01.03.2007 | Original Paper

Deoxycholate-Induced Colitis is Markedly Attenuated in Nos2 Knockout Mice in Association with Modulation of Gene Expression Profiles

verfasst von: Harris Bernstein, Hana Holubec, Carol Bernstein, Natalia A. Ignatenko, Eugene Gerner, Katerina Dvorak, David Besselsen, Karen Ann Blohm-Mangone, Jose Padilla-Torres, Barbora Dvorakova, Harinder Garewal, Claire M. Payne

Erschienen in: Digestive Diseases and Sciences | Ausgabe 3/2007

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Abstract

Nos2 knockout mice were compared to wild-type mice for susceptibility to colitis in response to a diet supplemented with deoxycholate, a bile acid increased in the colon of individuals on a high-fat diet. Wild-type mice fed a fat-related diet, supplemented with 0.2% DOC, develop colonic inflammation associated with increases in nitrosative stress, proliferation, oxidative DNA/RNA damage, and angiogenesis, as well as altered expression of numerous genes. However, Nos2 knockout mice fed a diet supplemented with deoxycholate were resistant to these alterations. In particular, 35 genes were identified whose expression was significantly altered at the mRNA level in deoxycholate-fed Nos2(+/+) mice but not in deoxycholate-fed Nos2(–/–) mice. Some of these alterations in NOS2-dependent gene expression correspond to those reported in human inflammatory bowel disease. Overall, our results indicate that NOS2 expression is necessary for the development of deoxycholate-induced colitis in mice, a unique dietary-related model of colitis.
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Metadaten
Titel
Deoxycholate-Induced Colitis is Markedly Attenuated in Nos2 Knockout Mice in Association with Modulation of Gene Expression Profiles
verfasst von
Harris Bernstein
Hana Holubec
Carol Bernstein
Natalia A. Ignatenko
Eugene Gerner
Katerina Dvorak
David Besselsen
Karen Ann Blohm-Mangone
Jose Padilla-Torres
Barbora Dvorakova
Harinder Garewal
Claire M. Payne
Publikationsdatum
01.03.2007
Erschienen in
Digestive Diseases and Sciences / Ausgabe 3/2007
Print ISSN: 0163-2116
Elektronische ISSN: 1573-2568
DOI
https://doi.org/10.1007/s10620-006-9608-0

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