RT Journal Article
SR Electronic
T1 Reduced susceptibility of mice overexpressing transforming growth factor α to dextran sodium sulphate induced colitis
JF Gut
JO Gut
FD BMJ Publishing Group Ltd and British Society of Gastroenterology
SP 64
OP 70
DO 10.1136/gut.43.1.64
VO 43
IS 1
A1 Egger, B
A1 Carey, H V
A1 Procaccino, F
A1 Chai, N-N
A1 Sandgren, E P
A1 Lakshmanan, J
A1 Buslon, V S
A1 French, S W
A1 Büchler, M W
A1 Eysselein, V E
YR 1998
UL http://gut.bmj.com/content/43/1/64.abstract
AB 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 ZnSO4administration in drinking water (TG+). Three groups were used as controls: one transgenic group without ZnSO4 administration (TG−), and two non-transgenic littermate groups receiving ZnSO4 (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.