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

被引：752

作者：

Ashcroft, GS

Yang, X

Glick, AB

Weinstein, M

Letterio, JJ

Mizel, DE

Anzano, M

Greenwell-Wild, T

Wahl, SM

Deng, CX

Roberts, AB

机构：

[1] NCI, Lab Cell Regulat & Carcinogenesis, Bethesda, MD 20892 USA

[2] NIDCR, Oral Infect & Immun Branch, NIH, Bethesda, MD 20892 USA

[3] NIDDK, Genet Dev & Dis Branch, NIH, Bethesda, MD 20892 USA

[4] NCI, Cellular Carcinogenesis & Tumor Promot Lab, NIH, Bethesda, MD 20892 USA

来源：

NATURE CELL BIOLOGY | 1999年 / 1卷 / 05期

基金：

英国惠康基金;

关键词：

D O I：

10.1038/12971

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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 (Smad3(ex8/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. Smad3(ex8/ex8) keratinocytes show altered patterns of growth and migration, and Smad3(ex8/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.

引用

页码：260 / 266

页数：7

共 33 条

[1] Estrogen accelerates cutaneous wound healing associated with an increase in TGF-beta 1 levels [J].