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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-47031

Bentz, S; Pesch, T; Wolfram, L; de Vallière, C; Leucht, K; Fried, M; Coy, J F; Hausmann, M; Rogler, G (2011). Lack of transketolase-like (TKTL) 1 aggravates murine experimental colitis. American Journal of Physiology. Gastrointestinal and Liver Physiology, 300(4):G598-G607.

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Abstract

Background: Transketolase-like (TKTL) 1 indirectly replenishes NADPH preventing damage induced by reactive oxygen species (ROS) formed upon intestinal inflammation. We investigated the function of TKTL1 during murine colitis and ROS detoxification for prevention of tissue damage. Methods: Mucosal damage in TKTL1(-/-) and wild type (WT) mice was assessed by miniendoscopy and histology during DSS colitis. mRNA levels of IFN-γ, iNOS, IL-6, TNF, transketolase (TKT) and TKTL2 were determined by PCR and/or Western blotting. To assess oxidative and nitrosative stress nitrosylation, carbonylation and anti-oxidative enzymes catalase (Cat), superoxide dismutase (SOD) 1 and 2 as well as glutathione (GSH) were determined. Myeloperoxidase (MPO) was determined for assessment of tissue neutrophils. Results: TKTL1 knock out or DSS treatment did not influence TKT and TKTL2 mRNA or protein expression. Mucosal damage was significantly increased in TKTL1(-/-) mice indicated by miniendoscopy as well as a significant shorter colon and more severe histological scores compared to WT mice during DSS colitis. This was associated with higher mRNA levels of IFN-γ, iNOS, IL-6 and TNF. In addition, iNOS protein expression was significantly enhanced in TKTL1(-/-) mice as well as MPO activity. Protein modification by NO (N-Tyr) was induced in TKTL1(-/-) mice. However, introduction of carbonylgroups by ROS was not induced in these mice. The expression of SOD1, SOD2, Cat as well as GSH content were not significantly changed in TKTL1(-/-) mice. Conclusion: Induced colitis in TKTL1(-/-) mice was more severe as compared to WT. This indicates a role of TKTL1 during mucosal repair and restoration.

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Physiology
07 Faculty of Science > Institute of Physiology

04 Faculty of Medicine > University Hospital Zurich > Clinic for Gastroenterology and Hepatology
DDC:570 Life sciences; biology
610 Medicine & health
Date:2011
Deposited On:07 Mar 2011 15:57
Last Modified:27 Nov 2013 20:22
Publisher:American Physiological Society
ISSN:0193-1857
Publisher DOI:10.1152/ajpgi.00323.2010
PubMed ID:21233279
Citations:Web of Science®. Times Cited: 1
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Scopus®. Citation Count: 2

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