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Hypertrophic scar regression is linked to the occurrence of endothelial dysfunction

Most microvessels have been shown to become stenosed or completely occluded during hypertrophic scar progression. Here, we examined the morphology of capillary endothelial cells (ECs) and fibroblasts using immunofluorescence staining for CD31 and alpha-smooth muscle actin (α-SMA) and electron micros...

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Autores principales: Wang, Xi-Qiao, Song, Fei, Liu, Ying-Kai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5417599/
https://www.ncbi.nlm.nih.gov/pubmed/28472181
http://dx.doi.org/10.1371/journal.pone.0176681
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author Wang, Xi-Qiao
Song, Fei
Liu, Ying-Kai
author_facet Wang, Xi-Qiao
Song, Fei
Liu, Ying-Kai
author_sort Wang, Xi-Qiao
collection PubMed
description Most microvessels have been shown to become stenosed or completely occluded during hypertrophic scar progression. Here, we examined the morphology of capillary endothelial cells (ECs) and fibroblasts using immunofluorescence staining for CD31 and alpha-smooth muscle actin (α-SMA) and electron microscopy. In addition, ECs and fibroblasts were isolated from scar tissues, and the levels of transforming growth factor beta 1 (TGF-β1), platelet-derived growth factor (PDGF), endothelin 1 (ET-1), vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) were assayed using ELISAs. Furthermore, we assessed cell viability, total collagen production, and cell apoptosis in hypertrophic scar-derived fibroblasts cultured with EC-conditioned medium. Then, anti-TGF-β1, anti-PDGF, anti-ET-1, anti-VEGF, and anti-bFGF neutralising antibodies were individually added to the EC medium to identify which growth factor plays a more important role in inhibiting fibroblasts biology. Our results showed microvessel lumen occlusion and EC atrophy during scar development, particularly in regressive scars (RSs). Additionally, EC growth factor secretion decreased and reached the lowest levels in RSs. Furthermore, based on the culture results, RS EC medium inhibited fibroblast viability and collagen production and induced apoptosis. Moreover, TGF-β1, PDGF, and bFGF played more important roles in these processes than VEGF and ET-1. The endothelial dysfunction occurring in hypertrophic scars contributes to fibroblast inhibition and scar regression, and reduced TGF-β1, PDGF, and bFGF levels play key roles during this process.
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spelling pubmed-54175992017-05-14 Hypertrophic scar regression is linked to the occurrence of endothelial dysfunction Wang, Xi-Qiao Song, Fei Liu, Ying-Kai PLoS One Research Article Most microvessels have been shown to become stenosed or completely occluded during hypertrophic scar progression. Here, we examined the morphology of capillary endothelial cells (ECs) and fibroblasts using immunofluorescence staining for CD31 and alpha-smooth muscle actin (α-SMA) and electron microscopy. In addition, ECs and fibroblasts were isolated from scar tissues, and the levels of transforming growth factor beta 1 (TGF-β1), platelet-derived growth factor (PDGF), endothelin 1 (ET-1), vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) were assayed using ELISAs. Furthermore, we assessed cell viability, total collagen production, and cell apoptosis in hypertrophic scar-derived fibroblasts cultured with EC-conditioned medium. Then, anti-TGF-β1, anti-PDGF, anti-ET-1, anti-VEGF, and anti-bFGF neutralising antibodies were individually added to the EC medium to identify which growth factor plays a more important role in inhibiting fibroblasts biology. Our results showed microvessel lumen occlusion and EC atrophy during scar development, particularly in regressive scars (RSs). Additionally, EC growth factor secretion decreased and reached the lowest levels in RSs. Furthermore, based on the culture results, RS EC medium inhibited fibroblast viability and collagen production and induced apoptosis. Moreover, TGF-β1, PDGF, and bFGF played more important roles in these processes than VEGF and ET-1. The endothelial dysfunction occurring in hypertrophic scars contributes to fibroblast inhibition and scar regression, and reduced TGF-β1, PDGF, and bFGF levels play key roles during this process. Public Library of Science 2017-05-04 /pmc/articles/PMC5417599/ /pubmed/28472181 http://dx.doi.org/10.1371/journal.pone.0176681 Text en © 2017 Wang et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Wang, Xi-Qiao
Song, Fei
Liu, Ying-Kai
Hypertrophic scar regression is linked to the occurrence of endothelial dysfunction
title Hypertrophic scar regression is linked to the occurrence of endothelial dysfunction
title_full Hypertrophic scar regression is linked to the occurrence of endothelial dysfunction
title_fullStr Hypertrophic scar regression is linked to the occurrence of endothelial dysfunction
title_full_unstemmed Hypertrophic scar regression is linked to the occurrence of endothelial dysfunction
title_short Hypertrophic scar regression is linked to the occurrence of endothelial dysfunction
title_sort hypertrophic scar regression is linked to the occurrence of endothelial dysfunction
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5417599/
https://www.ncbi.nlm.nih.gov/pubmed/28472181
http://dx.doi.org/10.1371/journal.pone.0176681
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