We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response.
- Authors
Ashcroft, G S; Yang, X; Glick, A B; Weinstein, M; Letterio, J L; Mizel, D E; Anzano, M; Greenwell-Wild, T; Wahl, S M; Deng, C; Roberts, A B
- Abstract
The generation of animals lacking SMAD proteins, which transduce signals from transforming growth factor-beta (TGF-beta), has made it possible to explore the contribution of the SMAD proteins to TGF-beta activity in vivo. Here we report that, in contrast to predictions made on the basis of the ability of exogenous TGF-beta to improve wound healing, Smad3-null (Smad3ex8/ex8) mice paradoxically show accelerated cutaneous wound healing compared with wild-type mice, characterized by an increased rate of re-epithelialization and significantly reduced local infiltration of monocytes. Smad3ex8/ex8 keratinocytes show altered patterns of growth and migration, and Smad3ex8/ex8 monocytes exhibit a selectively blunted chemotactic response to TGF-beta. These data are, to our knowledge, the first to implicate Smad3 in specific pathways of tissue repair and in the modulation of keratinocyte and monocyte function in vivo.
- Publication
Nature cell biology, 1999, Vol 1, Issue 5, p260
- ISSN
1465-7392
- Publication type
Journal Article
- DOI
10.1038/12971