| First Author | Ashcroft GS | Year | 1999 |
| Journal | Nat Cell Biol | Volume | 1 |
| Issue | 5 | Pages | 260-6 |
| PubMed ID | 10559937 | Mgi Jnum | J:59673 |
| Mgi Id | MGI:1352043 | Doi | 10.1038/12971 |
| Citation | Ashcroft GS, et al. (1999) Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response [see comments]. Nat Cell Biol 1(5):260-6 |
| abstractText | 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. |
