Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response - PubMed (original) (raw)

Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response

G S Ashcroft et al. Nat Cell Biol. 1999 Sep.

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.

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Comment in

• Wounding Smad.
  Massagué J. Massagué J. Nat Cell Biol. 1999 Sep;1(5):E117-9. doi: 10.1038/12944. Nat Cell Biol. 1999. PMID: 10559949 No abstract available.

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