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Downregulation of miR-27b promotes skin wound healing in a rat model of scald burn by promoting fibroblast proliferation

The aim of the present study was to investigate the effect and mechanism of action of microRNA (miR)-27b on skin wound healing in rats with deep second-degree scald burns and in BJ human skin fibroblast cells. Rat models with deep second-degree scald burns were constructed and injected with miR-27b...

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Autores principales: Bi, Qingxia, Liu, Jingyan, Wang, Xueming, Sun, Furong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7485298/
https://www.ncbi.nlm.nih.gov/pubmed/32952653
http://dx.doi.org/10.3892/etm.2020.9191
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author Bi, Qingxia
Liu, Jingyan
Wang, Xueming
Sun, Furong
author_facet Bi, Qingxia
Liu, Jingyan
Wang, Xueming
Sun, Furong
author_sort Bi, Qingxia
collection PubMed
description The aim of the present study was to investigate the effect and mechanism of action of microRNA (miR)-27b on skin wound healing in rats with deep second-degree scald burns and in BJ human skin fibroblast cells. Rat models with deep second-degree scald burns were constructed and injected with miR-27b mimics and inhibitors at the wound site daily for 21 days. Healing of burned skin tissues was observed at 0, 3, 7, 14 and 21 days following modeling. H&E and Masson staining were used to observe the pathological structure and degree of collagen fibers in the burned skin tissues. The effects of miR-27b on BJ cell proliferation and migration were determined by MTT and scratch assays. Matrix metalloproteinase-1 (MMP-1), α-smooth muscle actin (α-SMA), collagen I and collagen III expression in rat skin tissues and BJ cells were measured via reverse transcription-quantitative PCR and western blot analysis. The results of the in vivo experiments demonstrated that miR-27b inhibition accelerated scalded skin healing and induced fibroblast growth. Furthermore, the in vitro experiments revealed that miR-27b inhibition increased BJ cell proliferation and migration. Furthermore, miR-27b inhibition upregulated MMP-1, α-SMA, collagen I and collagen III expression in the skin tissues and cells, while the overexpression of miR-27b demonstrated the opposite effect. In conclusion, the results of the present study revealed that miR-27b inhibition increased fibroblast proliferation, thereby accelerating scald wound healing in rats.
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spelling pubmed-74852982020-09-18 Downregulation of miR-27b promotes skin wound healing in a rat model of scald burn by promoting fibroblast proliferation Bi, Qingxia Liu, Jingyan Wang, Xueming Sun, Furong Exp Ther Med Articles The aim of the present study was to investigate the effect and mechanism of action of microRNA (miR)-27b on skin wound healing in rats with deep second-degree scald burns and in BJ human skin fibroblast cells. Rat models with deep second-degree scald burns were constructed and injected with miR-27b mimics and inhibitors at the wound site daily for 21 days. Healing of burned skin tissues was observed at 0, 3, 7, 14 and 21 days following modeling. H&E and Masson staining were used to observe the pathological structure and degree of collagen fibers in the burned skin tissues. The effects of miR-27b on BJ cell proliferation and migration were determined by MTT and scratch assays. Matrix metalloproteinase-1 (MMP-1), α-smooth muscle actin (α-SMA), collagen I and collagen III expression in rat skin tissues and BJ cells were measured via reverse transcription-quantitative PCR and western blot analysis. The results of the in vivo experiments demonstrated that miR-27b inhibition accelerated scalded skin healing and induced fibroblast growth. Furthermore, the in vitro experiments revealed that miR-27b inhibition increased BJ cell proliferation and migration. Furthermore, miR-27b inhibition upregulated MMP-1, α-SMA, collagen I and collagen III expression in the skin tissues and cells, while the overexpression of miR-27b demonstrated the opposite effect. In conclusion, the results of the present study revealed that miR-27b inhibition increased fibroblast proliferation, thereby accelerating scald wound healing in rats. D.A. Spandidos 2020-11 2020-09-04 /pmc/articles/PMC7485298/ /pubmed/32952653 http://dx.doi.org/10.3892/etm.2020.9191 Text en Copyright: © Bi et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Bi, Qingxia
Liu, Jingyan
Wang, Xueming
Sun, Furong
Downregulation of miR-27b promotes skin wound healing in a rat model of scald burn by promoting fibroblast proliferation
title Downregulation of miR-27b promotes skin wound healing in a rat model of scald burn by promoting fibroblast proliferation
title_full Downregulation of miR-27b promotes skin wound healing in a rat model of scald burn by promoting fibroblast proliferation
title_fullStr Downregulation of miR-27b promotes skin wound healing in a rat model of scald burn by promoting fibroblast proliferation
title_full_unstemmed Downregulation of miR-27b promotes skin wound healing in a rat model of scald burn by promoting fibroblast proliferation
title_short Downregulation of miR-27b promotes skin wound healing in a rat model of scald burn by promoting fibroblast proliferation
title_sort downregulation of mir-27b promotes skin wound healing in a rat model of scald burn by promoting fibroblast proliferation
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7485298/
https://www.ncbi.nlm.nih.gov/pubmed/32952653
http://dx.doi.org/10.3892/etm.2020.9191
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