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Comparative transcriptomic profiling of hydrogen peroxide signaling networks in zebrafish and human keratinocytes: Implications toward conservation, migration and wound healing

Skin wounds need to be repaired rapidly after injury to restore proper skin barrier function. Hydrogen peroxide (H(2)O(2)) is a conserved signaling factor that has been shown to promote a variety of skin wound repair processes, including immune cell migration, angiogenesis and sensory axon repair. D...

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Autores principales: Lisse, Thomas S., King, Benjamin L., Rieger, Sandra
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4742856/
https://www.ncbi.nlm.nih.gov/pubmed/26846883
http://dx.doi.org/10.1038/srep20328
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author Lisse, Thomas S.
King, Benjamin L.
Rieger, Sandra
author_facet Lisse, Thomas S.
King, Benjamin L.
Rieger, Sandra
author_sort Lisse, Thomas S.
collection PubMed
description Skin wounds need to be repaired rapidly after injury to restore proper skin barrier function. Hydrogen peroxide (H(2)O(2)) is a conserved signaling factor that has been shown to promote a variety of skin wound repair processes, including immune cell migration, angiogenesis and sensory axon repair. Despite growing research on H(2)O(2) functions in wound repair, the downstream signaling pathways activated by this reactive oxygen species in the context of injury remain largely unknown. The goal of this study was to provide a comprehensive analysis of gene expression changes in the epidermis upon exposure to H(2)O(2) concentrations known to promote wound repair. Comparative transcriptome analysis using RNA-seq data from larval zebrafish and previously reported microarray data from a human epidermal keratinocyte line shows that H(2)O(2) activates conserved cell migration, adhesion, cytoprotective and anti-apoptotic programs in both zebrafish and human keratinocytes. Further assessment of expression characteristics and signaling pathways revealed the activation of three major H(2)O(2)–dependent pathways, EGF, FOXO1, and IKKα. This study expands on our current understanding of the clinical potential of low-level H(2)O(2) for the promotion of epidermal wound repair and provides potential candidates in the treatment of wound healing deficits.
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spelling pubmed-47428562016-02-09 Comparative transcriptomic profiling of hydrogen peroxide signaling networks in zebrafish and human keratinocytes: Implications toward conservation, migration and wound healing Lisse, Thomas S. King, Benjamin L. Rieger, Sandra Sci Rep Article Skin wounds need to be repaired rapidly after injury to restore proper skin barrier function. Hydrogen peroxide (H(2)O(2)) is a conserved signaling factor that has been shown to promote a variety of skin wound repair processes, including immune cell migration, angiogenesis and sensory axon repair. Despite growing research on H(2)O(2) functions in wound repair, the downstream signaling pathways activated by this reactive oxygen species in the context of injury remain largely unknown. The goal of this study was to provide a comprehensive analysis of gene expression changes in the epidermis upon exposure to H(2)O(2) concentrations known to promote wound repair. Comparative transcriptome analysis using RNA-seq data from larval zebrafish and previously reported microarray data from a human epidermal keratinocyte line shows that H(2)O(2) activates conserved cell migration, adhesion, cytoprotective and anti-apoptotic programs in both zebrafish and human keratinocytes. Further assessment of expression characteristics and signaling pathways revealed the activation of three major H(2)O(2)–dependent pathways, EGF, FOXO1, and IKKα. This study expands on our current understanding of the clinical potential of low-level H(2)O(2) for the promotion of epidermal wound repair and provides potential candidates in the treatment of wound healing deficits. Nature Publishing Group 2016-02-05 /pmc/articles/PMC4742856/ /pubmed/26846883 http://dx.doi.org/10.1038/srep20328 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Lisse, Thomas S.
King, Benjamin L.
Rieger, Sandra
Comparative transcriptomic profiling of hydrogen peroxide signaling networks in zebrafish and human keratinocytes: Implications toward conservation, migration and wound healing
title Comparative transcriptomic profiling of hydrogen peroxide signaling networks in zebrafish and human keratinocytes: Implications toward conservation, migration and wound healing
title_full Comparative transcriptomic profiling of hydrogen peroxide signaling networks in zebrafish and human keratinocytes: Implications toward conservation, migration and wound healing
title_fullStr Comparative transcriptomic profiling of hydrogen peroxide signaling networks in zebrafish and human keratinocytes: Implications toward conservation, migration and wound healing
title_full_unstemmed Comparative transcriptomic profiling of hydrogen peroxide signaling networks in zebrafish and human keratinocytes: Implications toward conservation, migration and wound healing
title_short Comparative transcriptomic profiling of hydrogen peroxide signaling networks in zebrafish and human keratinocytes: Implications toward conservation, migration and wound healing
title_sort comparative transcriptomic profiling of hydrogen peroxide signaling networks in zebrafish and human keratinocytes: implications toward conservation, migration and wound healing
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4742856/
https://www.ncbi.nlm.nih.gov/pubmed/26846883
http://dx.doi.org/10.1038/srep20328
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