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A “traffic control” role for TGFβ3: orchestrating dermal and epidermal cell motility during wound healing
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...
Autores principales: | , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
2006
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2063766/ https://www.ncbi.nlm.nih.gov/pubmed/16549496 http://dx.doi.org/10.1083/jcb.200507111 |
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author | Bandyopadhyay, Balaji Fan, Jianhua Guan, Shengxi Li, Yong Chen, Mei Woodley, David T. Li, Wei |
author_facet | Bandyopadhyay, Balaji Fan, Jianhua Guan, Shengxi Li, Yong Chen, Mei Woodley, David T. Li, Wei |
author_sort | Bandyopadhyay, Balaji |
collection | PubMed |
description | 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. |
format | Text |
id | pubmed-2063766 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2006 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-20637662007-11-29 A “traffic control” role for TGFβ3: orchestrating dermal and epidermal cell motility during wound healing Bandyopadhyay, Balaji Fan, Jianhua Guan, Shengxi Li, Yong Chen, Mei Woodley, David T. Li, Wei J Cell Biol Research Articles 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. The Rockefeller University Press 2006-03-27 /pmc/articles/PMC2063766/ /pubmed/16549496 http://dx.doi.org/10.1083/jcb.200507111 Text en Copyright © 2006, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Research Articles Bandyopadhyay, Balaji Fan, Jianhua Guan, Shengxi Li, Yong Chen, Mei Woodley, David T. Li, Wei A “traffic control” role for TGFβ3: orchestrating dermal and epidermal cell motility during wound healing |
title | A “traffic control” role for TGFβ3: orchestrating dermal and epidermal cell motility during wound healing |
title_full | A “traffic control” role for TGFβ3: orchestrating dermal and epidermal cell motility during wound healing |
title_fullStr | A “traffic control” role for TGFβ3: orchestrating dermal and epidermal cell motility during wound healing |
title_full_unstemmed | A “traffic control” role for TGFβ3: orchestrating dermal and epidermal cell motility during wound healing |
title_short | A “traffic control” role for TGFβ3: orchestrating dermal and epidermal cell motility during wound healing |
title_sort | “traffic control” role for tgfβ3: orchestrating dermal and epidermal cell motility during wound healing |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2063766/ https://www.ncbi.nlm.nih.gov/pubmed/16549496 http://dx.doi.org/10.1083/jcb.200507111 |
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