Smad3 knockout mice exhibit impaired intestinal mucosal healing.

Laboratory Investigation; a Journal of Technical Methods and Pathology
Cheri R OwenMarc D Basson

Abstract

Altered transforming growth factor-beta (TGFbeta) expression may contribute to inflammatory bowel disease and modulate epithelial cell restitution. Interference with TGFbeta-mediated signaling inhibits excisional skin wound healing, but accelerates healing of incisional cutaneous wounds and wounds in some other tissues. Therefore, we sought to clarify the potential role of Smad3-dependent TGFbeta signaling in intestinal mucosal healing in Smad3 null mice. Jejunal serosal application of filter disks saturated with 75% acetic acid yielded a circumscribed reproducible ischemic mucosal ulcer 1 day later. We compared ulcer area at 3 and 5 days to day 1 in Smad3 knockout mice and syngeneic wild-type mice, and evaluated mucosal immunoreactivity at the ulcer edge for TGFbeta, phosphorylated (activated) focal adhesion kinase (pFAK), phosphorylated extracellular signal-related kinase (pERK), proliferating cell nuclear antigen and apoptosis by TUNEL. Ulcer healing in Smad3 null mice was 17% less at day 3 (n=14, P=0.022) and 15% less at day 5 (n=14, P=0.004) than in wild-type littermates. In wild-type mice, pFAK, pERK and TGFbeta immunoreactivity were elevated in epithelium immediately adjacent to the ulcer compared with more distant mucos...Continue Reading

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Citations

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Mar 3, 2009·Cellular Signalling·Christopher P Gayer, Marc D Basson

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