缺乏Smad3的小鼠伤口愈合加速且局部炎症反应受损。
Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response.
作者信息
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
机构信息
Laboratory of Cell Regulation and Carcinogenesis, NCI, Bethesda, Maryland 20892-5055, USA.
出版信息
Nat Cell Biol. 1999 Sep;1(5):260-6. doi: 10.1038/12971.
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.
缺乏SMAD蛋白（其可转导来自转化生长因子-β（TGF-β）的信号）的动物的产生，使得探索SMAD蛋白在体内对TGF-β活性的贡献成为可能。我们在此报告，与基于外源性TGF-β改善伤口愈合能力所做的预测相反，与野生型小鼠相比，Smad3基因敲除（Smad3ex8/ex8）小鼠的皮肤伤口愈合反而加速，其特征为再上皮化速率增加且单核细胞局部浸润显著减少。Smad3ex8/ex8角质形成细胞显示出生长和迁移模式的改变，并且Smad3ex8/ex8单核细胞对TGF-β表现出选择性减弱的趋化反应。据我们所知，这些数据首次表明Smad3参与体内组织修复的特定途径以及角质形成细胞和单核细胞功能的调节。
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