Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response
Author: ["Gillian S. Ashcroft","Xiao Yang","Adam B. Glick","Michael Weinstein","John J. Letterio","Diane E. Mizel","Mario Anzano","Teresa Greenwell-Wild","Sharon M. Wahl","Chuxia Deng","Anita B. Roberts"]
Publication: Nature Cell Biology
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Abstract
The generation of animals lacking SMAD proteins, which transduce signals from transforming growth factor-β (TGF-β), has made it possible to explore the contribution of the SMAD proteins to TGF-β activity in vivo. Here we report that, in contrast to predictions made on the basis of the ability of exogenous TGF-β 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-β. 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.
Cite this article
Ashcroft, G., Yang, X., Glick, A. et al. Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response. Nat Cell Biol 1, 260–266 (1999). https://doi.org/10.1038/12971
