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Ashcroft, G.S. et al.

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

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.[1]

References

Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response. 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. Nat. Cell Biol. (1999) [Pubmed]

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