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MicroRNA-185 regulates transforming growth factor-β1 and collagen-1 in hypertrophic scar fibroblasts
Transforming growth factor-β1 (TGF-β1) and collagen type I (Col-1) serve a critical role in the development and progression of hypertrophic scarring (HS). The present study hypothesized that a post-translational mechanism of microRNAs (miR) regulated the expression of TGF-β1 and Col-1 in HS fibrobla...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5364971/ https://www.ncbi.nlm.nih.gov/pubmed/28259900 http://dx.doi.org/10.3892/mmr.2017.6179 |
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author | Xiao, Kaiyan Luo, Xusong Wang, Xiuxia Gao, Zhen |
author_facet | Xiao, Kaiyan Luo, Xusong Wang, Xiuxia Gao, Zhen |
author_sort | Xiao, Kaiyan |
collection | PubMed |
description | Transforming growth factor-β1 (TGF-β1) and collagen type I (Col-1) serve a critical role in the development and progression of hypertrophic scarring (HS). The present study hypothesized that a post-translational mechanism of microRNAs (miR) regulated the expression of TGF-β1 and Col-1 in HS fibroblasts (HSFBs). A collection of 20 HS tissues was compared with corresponding normal tissues from clinical patients, and the expression of miR-185 was measured. Using PicTar, TargetScan and miRBase databases, it was identified that miR-185 may be a regulator of TGF-β1 and Col-1 in humans. Based on these hypotheses, the expression of miR-185, TGF-β1 and Col-1 in HS tissues was investigated. The results demonstrated that the expression of miR-185 was markedly suppressed, and TGF-β1 and Col-1 levels were increased, in HS tissues. The expression levels of endogenous miR-185 negatively correlated with the TGF-β1 and Col-1 mRNA levels (Pearson's correlation coefficient r=−0.674, P<0.01 and r=−0.590, P<0.01, respectively). In vitro, miR-185 can regulate TGF-β1 and Col-1 through the predicted binding sites in its 3′-untranslated region. miR-185 had an effect on cell proliferation and apoptosis, thereby regulating HSFBs growth. In addition, miR-185 gain-of-function decreased TGF-β1 and Col-1 protein expression, and miR-185 loss-of-function increased TGF-β1 and Col-1 protein expression in HSFBs. In conclusion, overexpressed miR-185 could inhibit HSFBs growth, and the underlying mechanism was mediated, at least partly, through the suppression of TGF-β1 and Col-1 expression. However, above all, miR-185 might serve as a potential therapeutic approach for the treatment of HS. |
format | Online Article Text |
id | pubmed-5364971 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-53649712017-05-15 MicroRNA-185 regulates transforming growth factor-β1 and collagen-1 in hypertrophic scar fibroblasts Xiao, Kaiyan Luo, Xusong Wang, Xiuxia Gao, Zhen Mol Med Rep Articles Transforming growth factor-β1 (TGF-β1) and collagen type I (Col-1) serve a critical role in the development and progression of hypertrophic scarring (HS). The present study hypothesized that a post-translational mechanism of microRNAs (miR) regulated the expression of TGF-β1 and Col-1 in HS fibroblasts (HSFBs). A collection of 20 HS tissues was compared with corresponding normal tissues from clinical patients, and the expression of miR-185 was measured. Using PicTar, TargetScan and miRBase databases, it was identified that miR-185 may be a regulator of TGF-β1 and Col-1 in humans. Based on these hypotheses, the expression of miR-185, TGF-β1 and Col-1 in HS tissues was investigated. The results demonstrated that the expression of miR-185 was markedly suppressed, and TGF-β1 and Col-1 levels were increased, in HS tissues. The expression levels of endogenous miR-185 negatively correlated with the TGF-β1 and Col-1 mRNA levels (Pearson's correlation coefficient r=−0.674, P<0.01 and r=−0.590, P<0.01, respectively). In vitro, miR-185 can regulate TGF-β1 and Col-1 through the predicted binding sites in its 3′-untranslated region. miR-185 had an effect on cell proliferation and apoptosis, thereby regulating HSFBs growth. In addition, miR-185 gain-of-function decreased TGF-β1 and Col-1 protein expression, and miR-185 loss-of-function increased TGF-β1 and Col-1 protein expression in HSFBs. In conclusion, overexpressed miR-185 could inhibit HSFBs growth, and the underlying mechanism was mediated, at least partly, through the suppression of TGF-β1 and Col-1 expression. However, above all, miR-185 might serve as a potential therapeutic approach for the treatment of HS. D.A. Spandidos 2017-04 2017-02-08 /pmc/articles/PMC5364971/ /pubmed/28259900 http://dx.doi.org/10.3892/mmr.2017.6179 Text en Copyright: © Xiao 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 Xiao, Kaiyan Luo, Xusong Wang, Xiuxia Gao, Zhen MicroRNA-185 regulates transforming growth factor-β1 and collagen-1 in hypertrophic scar fibroblasts |
title | MicroRNA-185 regulates transforming growth factor-β1 and collagen-1 in hypertrophic scar fibroblasts |
title_full | MicroRNA-185 regulates transforming growth factor-β1 and collagen-1 in hypertrophic scar fibroblasts |
title_fullStr | MicroRNA-185 regulates transforming growth factor-β1 and collagen-1 in hypertrophic scar fibroblasts |
title_full_unstemmed | MicroRNA-185 regulates transforming growth factor-β1 and collagen-1 in hypertrophic scar fibroblasts |
title_short | MicroRNA-185 regulates transforming growth factor-β1 and collagen-1 in hypertrophic scar fibroblasts |
title_sort | microrna-185 regulates transforming growth factor-β1 and collagen-1 in hypertrophic scar fibroblasts |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5364971/ https://www.ncbi.nlm.nih.gov/pubmed/28259900 http://dx.doi.org/10.3892/mmr.2017.6179 |
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