Cell migration is a rate-limiting event in skin wound healing. In unwounded skin, cells are nourished by plasma. When skin is wounded, resident cells encounter serum for the first time. As the wound heals, the cells experience a transition of serum back to plasma. In this study, we report that human serum selectively promotes epidermal cell migration and halts dermal cell migration. In contrast, human plasma promotes dermal but not epidermal cell migration. The on-and-off switch is operated by transforming growth factor (TGF) β3 levels, which are undetectable in plasma and high in serum, and by TGFβ receptor (TβR) type II levels, which are low in epidermal cells and high in dermal cells. Depletion of TGFβ3 from serum converts serum to a plasmalike reagent. The addition of TGFβ3 to plasma converts it to a serumlike reagent. Down-regulation of TβRII in dermal cells or up-regulation of TβRII in epidermal cells reverses their migratory responses to serum and plasma, respectively. Therefore, the naturally occurring plasma→serum→plasma transition during wound healing orchestrates the orderly migration of dermal and epidermal cells.
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27 March 2006
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March 20 2006
A “traffic control” role for TGFβ3: orchestrating dermal and epidermal cell motility during wound healing
Balaji Bandyopadhyay,
Balaji Bandyopadhyay
Department of Dermatology and Norris Comprehensive Cancer Center, University of Southern California Keck School of Medicine, Los Angeles, CA 90033
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Jianhua Fan,
Jianhua Fan
Department of Dermatology and Norris Comprehensive Cancer Center, University of Southern California Keck School of Medicine, Los Angeles, CA 90033
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Shengxi Guan,
Shengxi Guan
Department of Dermatology and Norris Comprehensive Cancer Center, University of Southern California Keck School of Medicine, Los Angeles, CA 90033
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Yong Li,
Yong Li
Department of Dermatology and Norris Comprehensive Cancer Center, University of Southern California Keck School of Medicine, Los Angeles, CA 90033
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Mei Chen,
Mei Chen
Department of Dermatology and Norris Comprehensive Cancer Center, University of Southern California Keck School of Medicine, Los Angeles, CA 90033
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David T. Woodley,
David T. Woodley
Department of Dermatology and Norris Comprehensive Cancer Center, University of Southern California Keck School of Medicine, Los Angeles, CA 90033
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Wei Li
Wei Li
Department of Dermatology and Norris Comprehensive Cancer Center, University of Southern California Keck School of Medicine, Los Angeles, CA 90033
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Balaji Bandyopadhyay
Department of Dermatology and Norris Comprehensive Cancer Center, University of Southern California Keck School of Medicine, Los Angeles, CA 90033
Jianhua Fan
Department of Dermatology and Norris Comprehensive Cancer Center, University of Southern California Keck School of Medicine, Los Angeles, CA 90033
Shengxi Guan
Department of Dermatology and Norris Comprehensive Cancer Center, University of Southern California Keck School of Medicine, Los Angeles, CA 90033
Yong Li
Department of Dermatology and Norris Comprehensive Cancer Center, University of Southern California Keck School of Medicine, Los Angeles, CA 90033
Mei Chen
Department of Dermatology and Norris Comprehensive Cancer Center, University of Southern California Keck School of Medicine, Los Angeles, CA 90033
David T. Woodley
Department of Dermatology and Norris Comprehensive Cancer Center, University of Southern California Keck School of Medicine, Los Angeles, CA 90033
Wei Li
Department of Dermatology and Norris Comprehensive Cancer Center, University of Southern California Keck School of Medicine, Los Angeles, CA 90033
Correspondence to Wei Li: [email protected]; or David T. Woodley: [email protected]
Abbreviations used in this paper: AG, average gap; BPE, bovine pituitary extract; DF, dermal fibroblast; GF, growth factor; HDMEC, human dermal microvascular endothelial cell; HK, human keratinocyte; MC, melanocyte; MI, migration index; siRNA, short inhibitory RNA; TβR, TGFβ receptor.
Received:
July 22 2005
Accepted:
February 21 2006
Online ISSN: 1540-8140
Print ISSN: 0021-9525
The Rockefeller University Press
2006
J Cell Biol (2006) 172 (7): 1093–1105.
Article history
Received:
July 22 2005
Accepted:
February 21 2006
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Serum keeps order in the wound
This article has been corrected
Correction: A “traffic control” role for TGFβ3: orchestrating dermal and epidermal cell motility during wound healing
Citation
Balaji Bandyopadhyay, Jianhua Fan, Shengxi Guan, Yong Li, Mei Chen, David T. Woodley, Wei Li; A “traffic control” role for TGFβ3: orchestrating dermal and epidermal cell motility during wound healing . J Cell Biol 27 March 2006; 172 (7): 1093–1105. doi: https://doi.org/10.1083/jcb.200507111
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