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- Title
Accelerated re-epithelialization inß<sub>3</sub>-integrin-deficient- mice is associated with enhanced TGF-ß1 signaling.
- Authors
Reynolds, L.E.; Conti, F.J.; Lucas, M.; Grose, R.; Robinson, S.; Stone, M.; Saunders, G.; Dickson, C.; Hynes, R.O.; Lacy-Hulbert, A.; Hodivala-Dilke, K.
- Abstract
The upregulation of TGF-ß1 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 lackingß3-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-ß1 and enhanced dermal fibroblast infiltration into wounds ofß3-null mice. Specifically,ß3-integrin deficiency is associated with elevated TGF-ßreceptor I and receptor II expression, reduced Smad3 levels, sustained Smad2 and Smad4 nuclear localization and enhanced TGF-ß1-mediated dermal fibroblast migration. These data indicate thatavß3-integrin can suppress TGF-ß1-mediated signaling, thereby controlling the rate of wound healing, and highlight a new mechanism for TGF-ß1 regulation byß3-integrins.
- Publication
Nature Medicine, 2005, Vol 11, Issue 2, p167
- ISSN
1078-8956
- Publication type
Academic Journal
- DOI
10.1038/nm1165