| First Author | Reynolds LE | Year | 2005 |
| Journal | Nat Med | Volume | 11 |
| Issue | 2 | Pages | 167-74 |
| PubMed ID | 15654327 | Mgi Jnum | J:96049 |
| Mgi Id | MGI:3528800 | Doi | 10.1038/nm1165 |
| Citation | Reynolds LE, et al. (2005) Accelerated re-epithelialization in beta(3)-integrin-deficient- mice is associated with enhanced TGF-beta1 signaling. Nat Med 11(2):167-174 |
| abstractText | The upregulation of TGF-beta1 and integrin expression during wound healing has implicated these molecules in this process, but their precise regulation and roles remain unclear. Here we report that, notably, mice lacking beta(3)-integrins show enhanced wound healing with re-epithelialization complete several days earlier than in wild-type mice. We show that this effect is the result of an increase in TGF-beta1 and enhanced dermal fibroblast infiltration into wounds of beta(3)-null mice. Specifically, beta(3)-integrin deficiency is associated with elevated TGF-beta receptor I and receptor II expression, reduced Smad3 levels, sustained Smad2 and Smad4 nuclear localization and enhanced TGF-beta1-mediated dermal fibroblast migration. These data indicate that alpha(v)beta(3)-integrin can suppress TGF-beta1-mediated signaling, thereby controlling the rate of wound healing, and highlight a new mechanism for TGF-beta1 regulation by beta(3)-integrins. |
