In:
Gut, BMJ, Vol. 43, No. 1 ( 1998-07-01), p. 64-70
Abstract:
Background —Transforming growth factor α (TGF-α) knockout mice have increased susceptibility to dextran sodium sulphate (DSS) induced colitis. Aim —To substantiate the findings that TGF-α is a key mediator of colonic mucosal protection and/or repair mechanisms by evaluating the susceptibility of mice overexpressing TGF-α to DSS induced colitis. Methods —TGF-α overexpression was induced in transgenic mice by ZnSO 4 administration in drinking water (TG+). Three groups were used as controls: one transgenic group without ZnSO 4 administration (TG−), and two non-transgenic littermate groups receiving ZnSO 4 (Non-TG+) or only water (Non-TG−). Acute colitis was induced in all groups by administration of DSS (5%, w/v) in drinking water for six days ad libitum. Results —About 35–39% of the entire colonic mucosa was destroyed in Non-TG−, Non-TG+, and TG− animals compared with 9% in TG+ mice. The crypt damage score was 18.7 (0.9), 18.2 (1.0), 18.9 (0.8), and 6.8 (1.5) (means (SEM)) in Non-TG−, Non-TG+, TG−, and TG+ mice respectively. Mucin and bromodeoxyuridine staining were markedly enhanced in colons of TG+ mice compared with controls, indicating increased mucosal protection and regeneration. Conclusions —The significantly reduced susceptibility of mice overexpressing TGF-α to DSS further substantiates that endogenous TGF-α is a pivotal mediator of protection and/or healing mechanisms in the colon.
Type of Medium:
Online Resource
ISSN:
0017-5749
,
1468-3288
Language:
English
Publisher:
BMJ
Publication Date:
1998
detail.hit.zdb_id:
1492637-4
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