Accelerated re-epithelialization in β3-integrin-deficient- mice is associated with enhanced TGF-β1 s
Author: ["L E Reynolds","F J Conti","M Lucas","R Grose","S Robinson","M Stone","G Saunders","C Dickson","R O Hynes","A Lacy-Hulbert","K Hodivala-Dilke"]
Publication: Nature Medicine
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Abstract
The upregulation of TGF-β1 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 β3-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-β1 and enhanced dermal fibroblast infiltration into wounds of β3-null mice. Specifically, β3-integrin deficiency is associated with elevated TGF-β receptor I and receptor II expression, reduced Smad3 levels, sustained Smad2 and Smad4 nuclear localization and enhanced TGF-β1-mediated dermal fibroblast migration. These data indicate that αvβ3–integrin can suppress TGF-β1-mediated signaling, thereby controlling the rate of wound healing, and highlight a new mechanism for TGF-β1 regulation by β3-integrins.
Cite this article
Reynolds, L., Conti, F., Lucas, M. et al. Accelerated re-epithelialization in β3-integrin-deficient- mice is associated with enhanced TGF-β1 signaling. Nat Med 11, 167–174 (2005). https://doi.org/10.1038/nm1165
