Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Subscribe

Logo for

J. Cell Biol. 172 (7): 1093-1105

Copyright © 2006 by the Rockefeller University Press.


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

Abstract: 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.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
TGF-{beta}3 modulates the inflammatory environment and reduces scar formation following vocal fold mucosal injury in rats.
Z. Chang, Y. Kishimoto, A. Hasan, and N. V. Welham (2014)
Dis. Model. Mech. 7, 83-91
   Abstract »    Full Text »    PDF »
Transforming Growth Factor-{beta}3 (TGF-{beta}3) Knock-in Ameliorates Inflammation Due to TGF-{beta}1 Deficiency While Promoting Glucose Tolerance.
B. E. Hall, U. D. Wankhade, J. E. Konkel, K. Cherukuri, C. N. Nagineni, K. C. Flanders, P. R. Arany, W. Chen, S. G. Rane, and A. B. Kulkarni (2013)
J. Biol. Chem. 288, 32074-32092
   Abstract »    Full Text »    PDF »
The anti-motility signaling mechanism of TGF{beta}3 that controls cell traffic during skin wound healing.
A. Han, B. Bandyopadhyay, P. Jayaprakash, I. Lua, D. Sahu, M. Chen, D. T. Woodley, and W. Li (2012)
Biology Open 1, 1169-1177
   Abstract »    Full Text »    PDF »
Photoactivated Composite Biomaterial for Soft Tissue Restoration in Rodents and in Humans.
A. T. Hillel, S. Unterman, Z. Nahas, B. Reid, J. M. Coburn, J. Axelman, J. J. Chae, Q. Guo, R. Trow, A. Thomas, et al. (2011)
Science Translational Medicine 3, 93ra67
   Abstract »    Full Text »    PDF »
T{beta}RI/Alk5-independent T{beta}RII signaling to ERK1/2 in human skin cells according to distinct levels of T{beta}RII expression.
B. Bandyopadhyay, A. Han, J. Dai, J. Fan, Y. Li, M. Chen, D. T. Woodley, and W. Li (2011)
J. Cell Sci. 124, 19-24
   Abstract »    Full Text »    PDF »
Target-seeking antifibrotic compound enhances wound healing and suppresses scar formation in mice.
T. A. H. Jarvinen and E. Ruoslahti (2010)
PNAS 107, 21671-21676
   Abstract »    Full Text »    PDF »
Calreticulin: non-endoplasmic reticulum functions in physiology and disease.
L. I. Gold, P. Eggleton, M. T. Sweetwyne, L. B. Van Duyn, M. R. Greives, S.-M. Naylor, M. Michalak, and J. E. Murphy-Ullrich (2010)
FASEB J 24, 665-683
   Abstract »    Full Text »    PDF »
Altered Molecular Mechanisms of Diabetic Foot Ulcers.
R. Blakytny and E. B. Jude (2009)
International Journal of Lower Extremity Wounds 8, 95-104
   Abstract »    PDF »
Avotermin: A Novel Antiscarring Agent.
P. Durani, N. Occleston, S. O'Kane, and M. W. J. Ferguson (2008)
International Journal of Lower Extremity Wounds 7, 160-168
   Abstract »    PDF »
Functional Characterization and Gene Expression Analysis of CD4+CD25+ Regulatory T Cells Generated in Mice Treated with 2,3,7,8-Tetrachlorodibenzo-p-Dioxin.
N. B. Marshall, W. R. Vorachek, L. B. Steppan, D. V. Mourich, and N. I. Kerkvliet (2008)
J. Immunol. 181, 2382-2391
   Abstract »    Full Text »    PDF »
Transforming Growth Factor {alpha} (TGF{alpha})-Stimulated Secretion of HSP90{alpha}: Using the Receptor LRP-1/CD91 To Promote Human Skin Cell Migration against a TGF{beta}-Rich Environment during Wound Healing.
C.-F. Cheng, J. Fan, M. Fedesco, S. Guan, Y. Li, B. Bandyopadhyay, A. M. Bright, D. Yerushalmi, M. Liang, M. Chen, et al. (2008)
Mol. Cell. Biol. 28, 3344-3358
   Abstract »    Full Text »    PDF »
Extracellular heat shock protein-90{alpha}: linking hypoxia to skin cell motility and wound healing.
W. Li, Y. Li, S. Guan, J. Fan, C.-F. Cheng, A. M. Bright, C. Chinn, M. Chen, and D. T. Woodley (2007)
EMBO J. 26, 1221-1233
   Abstract »    Full Text »    PDF »
A "traffic control" role for TGF{beta}3: orchestrating dermal and epidermal cell motility during wound healing.
B. Bandyopadhyay, J. Fan, S. Guan, Y. Li, M. Chen, D. T. Woodley, and W. Li (2006)
J. Exp. Med. 203, i11-11
   Full Text »

To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882