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β2AR Antagonists and β2AR Gene Deletion Both Promote Skin Wound Repair Processes

Skin wound healing is a complex process requiring the coordinated, temporal orchestration of numerous cell types and biological processes to regenerate damaged tissue. Previous work has demonstrated that a functional β-adrenergic receptor autocrine/paracrine network exists in skin, but the role of β...

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Autores principales: Pullar, Christine E, Le Provost, Gabrielle S, O'Leary, Andrew P, Evans, Sian E, Baier, Brian S, Isseroff, R Rivkah
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3396744/
https://www.ncbi.nlm.nih.gov/pubmed/22495178
http://dx.doi.org/10.1038/jid.2012.108
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author Pullar, Christine E
Le Provost, Gabrielle S
O'Leary, Andrew P
Evans, Sian E
Baier, Brian S
Isseroff, R Rivkah
author_facet Pullar, Christine E
Le Provost, Gabrielle S
O'Leary, Andrew P
Evans, Sian E
Baier, Brian S
Isseroff, R Rivkah
author_sort Pullar, Christine E
collection PubMed
description Skin wound healing is a complex process requiring the coordinated, temporal orchestration of numerous cell types and biological processes to regenerate damaged tissue. Previous work has demonstrated that a functional β-adrenergic receptor autocrine/paracrine network exists in skin, but the role of β2-adrenergic receptor (β2AR) in wound healing is unknown. A range of in vitro (single-cell migration, immunoblotting, ELISA, enzyme immunoassay), ex vivo (rat aortic ring assay), and in vivo (chick chorioallantoic membrane assay, zebrafish, murine wild-type, and β2AR knockout excisional skin wound models) models were used to demonstrate that blockade or loss of β2AR gene deletion promoted wound repair, a finding that is, to our knowledge, previously unreported. Compared with vehicle-only controls, β2AR antagonism increased angiogenesis, dermal fibroblast function, and re-epithelialization, but had no effect on wound inflammation in vivo. Skin wounds in β2AR knockout mice contracted and re-epithelialized faster in the first few days of wound repair in vivo. β2AR antagonism enhanced cell motility through distinct intracellular signalling mechanisms and increased vascular endothelial growth factor secretion from keratinocytes. β2AR antagonism promoted wound repair processes in the early stages of wound repair, revealing a possible new avenue for therapeutic intervention.
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spelling pubmed-33967442012-07-17 β2AR Antagonists and β2AR Gene Deletion Both Promote Skin Wound Repair Processes Pullar, Christine E Le Provost, Gabrielle S O'Leary, Andrew P Evans, Sian E Baier, Brian S Isseroff, R Rivkah J Invest Dermatol Original Article Skin wound healing is a complex process requiring the coordinated, temporal orchestration of numerous cell types and biological processes to regenerate damaged tissue. Previous work has demonstrated that a functional β-adrenergic receptor autocrine/paracrine network exists in skin, but the role of β2-adrenergic receptor (β2AR) in wound healing is unknown. A range of in vitro (single-cell migration, immunoblotting, ELISA, enzyme immunoassay), ex vivo (rat aortic ring assay), and in vivo (chick chorioallantoic membrane assay, zebrafish, murine wild-type, and β2AR knockout excisional skin wound models) models were used to demonstrate that blockade or loss of β2AR gene deletion promoted wound repair, a finding that is, to our knowledge, previously unreported. Compared with vehicle-only controls, β2AR antagonism increased angiogenesis, dermal fibroblast function, and re-epithelialization, but had no effect on wound inflammation in vivo. Skin wounds in β2AR knockout mice contracted and re-epithelialized faster in the first few days of wound repair in vivo. β2AR antagonism enhanced cell motility through distinct intracellular signalling mechanisms and increased vascular endothelial growth factor secretion from keratinocytes. β2AR antagonism promoted wound repair processes in the early stages of wound repair, revealing a possible new avenue for therapeutic intervention. Nature Publishing Group 2012-08 2012-04-12 /pmc/articles/PMC3396744/ /pubmed/22495178 http://dx.doi.org/10.1038/jid.2012.108 Text en Copyright © 2012 The Society for Investigative Dermatology, Inc http://creativecommons.org/licenses/by-nc-nd/3.0/ This work is licensed under the Creative Commons Attribution-NonCommercial-No Derivative Works 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/
spellingShingle Original Article
Pullar, Christine E
Le Provost, Gabrielle S
O'Leary, Andrew P
Evans, Sian E
Baier, Brian S
Isseroff, R Rivkah
β2AR Antagonists and β2AR Gene Deletion Both Promote Skin Wound Repair Processes
title β2AR Antagonists and β2AR Gene Deletion Both Promote Skin Wound Repair Processes
title_full β2AR Antagonists and β2AR Gene Deletion Both Promote Skin Wound Repair Processes
title_fullStr β2AR Antagonists and β2AR Gene Deletion Both Promote Skin Wound Repair Processes
title_full_unstemmed β2AR Antagonists and β2AR Gene Deletion Both Promote Skin Wound Repair Processes
title_short β2AR Antagonists and β2AR Gene Deletion Both Promote Skin Wound Repair Processes
title_sort β2ar antagonists and β2ar gene deletion both promote skin wound repair processes
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3396744/
https://www.ncbi.nlm.nih.gov/pubmed/22495178
http://dx.doi.org/10.1038/jid.2012.108
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