| First Author | Tokumasa A | Year | 2004 |
| Journal | Biochem Biophys Res Commun | Volume | 317 |
| Issue | 2 | Pages | 377-83 |
| PubMed ID | 15063768 | Mgi Jnum | J:89177 |
| Mgi Id | MGI:3038594 | Doi | 10.1016/j.bbrc.2004.03.047 |
| Citation | Tokumasa A, et al. (2004) Reduction of Smad3 accelerates re-epithelialization in a murine model of colitis. Biochem Biophys Res Commun 317(2):377-83 |
| abstractText | To determine the role of Smad3 in re-epithelialization and inflammation, experimental colitis was induced in Smad3 heterozygous mice and their wild-type littermates by single intrarectal administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) in ethanol. The area of epithelial deficiency was significantly reduced in the heterozygotes on the 4th-6th day after TNBS administration as compared to the controls although the number of inflammatory cells in the colonic mucosa in the heterozygotes and their wild-type littermates varied similarly throughout the course of colitis. Proliferation of the intestinal epithelium in the heterozygotes was significantly accelerated as compared to that in the wild-type controls on the 1st and 2nd days after TNBS administration. These results suggest that reduction of Smad3 significantly accelerates re-epithelialization of the intestinal mucosa without enhancing inflammation. Suppression of TGF-beta1 induction in the colonic mucosa of the heterozygotes may lead to a higher level of proliferation of intestinal epithelial cells. |
