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Published online 20 March 2006. doi:10.1083/jcb.200507111
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 172, Number 7, 1093-1105
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Article

 A "traffic control" role for TGFß3: orchestrating dermal and epidermal cell motility during wound healing

Balaji Bandyopadhyay, Jianhua Fan, Shengxi Guan, Yong Li, Mei Chen, David T. Woodley, and 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: wli{at}usc.edu; or David T. Woodley: dwoodley{at}usc.edu

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) ß3 levels, which are undetectable in plasma and high in serum, and by TGFß receptor (TßR) type II levels, which are low in epidermal cells and high in dermal cells. Depletion of TGFß3 from serum converts serum to a plasmalike reagent. The addition of TGFß3 to plasma converts it to a serumlike reagent. Down-regulation of TßRII in dermal cells or up-regulation of TßRII 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.

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; TßR, TGFß receptor.


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