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

Gillian Ashcroft; 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

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

Gillian Ashcroft, 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

Research output: Contribution to journal › Article › peer-review

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.

Original language	English
Pages (from-to)	260-266
Number of pages	6
Journal	Nature Cell Biology
Volume	1
Issue number	5
Publication status	Published - Sept 1999

Cite this

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title = "Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response",

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.",

author = "Gillian Ashcroft and Ashcroft, \{Gillian S.\} and Xiao Yang and Glick, \{Adam B.\} and Michael Weinstein and Letterio, \{John J.\} and Mizel, \{Diane E.\} and Mario Anzano and Teresa Greenwell-Wild and Wahl, \{Sharon M.\} and Chuxia Deng and Roberts, \{Anita B.\}",

year = "1999",

month = sep,

language = "English",

volume = "1",

pages = "260--266",

journal = "Nature Cell Biology",

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TY - JOUR

T1 - Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response

AU - Ashcroft, Gillian

AU - Ashcroft, Gillian S.

AU - Yang, Xiao

AU - Glick, Adam B.

AU - Weinstein, Michael

AU - Letterio, John J.

AU - Mizel, Diane E.

AU - Anzano, Mario

AU - Greenwell-Wild, Teresa

AU - Wahl, Sharon M.

AU - Deng, Chuxia

AU - Roberts, Anita B.

PY - 1999/9

Y1 - 1999/9

N2 - 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.

AB - 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.

UR - https://www.scopus.com/pages/publications/0033195998

M3 - Article

C2 - 10559937

SN - 1465-7392

VL - 1

SP - 260

EP - 266

JO - Nature Cell Biology

JF - Nature Cell Biology

IS - 5

ER -

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

Abstract

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