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MicroRNA-663 regulates the proliferation of fibroblasts in hypertrophic scars via transforming growth factor-β1
The present study determined the expression of microRNA (miR)-663 in hypertrophic scar (HS) tissues and investigate the regulatory mechanisms of miR-663 in HS. A total of 51 patients diagnosed with HS between December 2013 and February 2016 were included in the present study. HS tissues (experimenta...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6090240/ https://www.ncbi.nlm.nih.gov/pubmed/30116380 http://dx.doi.org/10.3892/etm.2018.6350 |
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author | Chen, Qi Zhao, Tianlan Xie, Xiaoming Yu, Daojiang Wu, Lijun Yu, Wenyuan Sun, Wei |
author_facet | Chen, Qi Zhao, Tianlan Xie, Xiaoming Yu, Daojiang Wu, Lijun Yu, Wenyuan Sun, Wei |
author_sort | Chen, Qi |
collection | PubMed |
description | The present study determined the expression of microRNA (miR)-663 in hypertrophic scar (HS) tissues and investigate the regulatory mechanisms of miR-663 in HS. A total of 51 patients diagnosed with HS between December 2013 and February 2016 were included in the present study. HS tissues (experimental group) and HS-adjacent tissues (control group) were collected. Primary fibroblasts were obtained from HS tissue and transfected with small-interfering RNA against transforming growth factor (TGF)-β1 or miR-663 mimics. Reverse-transcription quantitative PCR was used to determine the levels of TGF-β1 mRNA and miR-663. Western blot analysis was performed to determine TGF-β1 protein expression. An MTT assay was employed to detect the proliferation of fibroblasts, and a dual luciferase reporter assay was performed to identify the binding of miR-663 with TGF-β1 mRNA. TGF-β1 was found to have a regulatory role in HS at the transcriptional level. The expression of TGF-β1 was upregulated in HS tissues, and knockdown of TGF-β1 in cultured fibroblasts led to inhibition of proliferation. The expression of miR-663 was downregulated in HS. miR-663 was revealed to regulate the expression of TGF-β1 by binding with the 3′-untranslated region of TGF-β1 mRNA. Elevated expression of miR-663 inhibited the proliferation of fibroblasts by regulating TGF-β1 expression. The present study demonstrated that upregulation of TGF-β1 in HS tissues is associated with the downregulation of miR-663 expression. miR-663 may regulate the proliferation of fibroblasts in HS and the expression of associated proteins. |
format | Online Article Text |
id | pubmed-6090240 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-60902402018-08-16 MicroRNA-663 regulates the proliferation of fibroblasts in hypertrophic scars via transforming growth factor-β1 Chen, Qi Zhao, Tianlan Xie, Xiaoming Yu, Daojiang Wu, Lijun Yu, Wenyuan Sun, Wei Exp Ther Med Articles The present study determined the expression of microRNA (miR)-663 in hypertrophic scar (HS) tissues and investigate the regulatory mechanisms of miR-663 in HS. A total of 51 patients diagnosed with HS between December 2013 and February 2016 were included in the present study. HS tissues (experimental group) and HS-adjacent tissues (control group) were collected. Primary fibroblasts were obtained from HS tissue and transfected with small-interfering RNA against transforming growth factor (TGF)-β1 or miR-663 mimics. Reverse-transcription quantitative PCR was used to determine the levels of TGF-β1 mRNA and miR-663. Western blot analysis was performed to determine TGF-β1 protein expression. An MTT assay was employed to detect the proliferation of fibroblasts, and a dual luciferase reporter assay was performed to identify the binding of miR-663 with TGF-β1 mRNA. TGF-β1 was found to have a regulatory role in HS at the transcriptional level. The expression of TGF-β1 was upregulated in HS tissues, and knockdown of TGF-β1 in cultured fibroblasts led to inhibition of proliferation. The expression of miR-663 was downregulated in HS. miR-663 was revealed to regulate the expression of TGF-β1 by binding with the 3′-untranslated region of TGF-β1 mRNA. Elevated expression of miR-663 inhibited the proliferation of fibroblasts by regulating TGF-β1 expression. The present study demonstrated that upregulation of TGF-β1 in HS tissues is associated with the downregulation of miR-663 expression. miR-663 may regulate the proliferation of fibroblasts in HS and the expression of associated proteins. D.A. Spandidos 2018-08 2018-06-22 /pmc/articles/PMC6090240/ /pubmed/30116380 http://dx.doi.org/10.3892/etm.2018.6350 Text en Copyright: © Chen 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 Chen, Qi Zhao, Tianlan Xie, Xiaoming Yu, Daojiang Wu, Lijun Yu, Wenyuan Sun, Wei MicroRNA-663 regulates the proliferation of fibroblasts in hypertrophic scars via transforming growth factor-β1 |
title | MicroRNA-663 regulates the proliferation of fibroblasts in hypertrophic scars via transforming growth factor-β1 |
title_full | MicroRNA-663 regulates the proliferation of fibroblasts in hypertrophic scars via transforming growth factor-β1 |
title_fullStr | MicroRNA-663 regulates the proliferation of fibroblasts in hypertrophic scars via transforming growth factor-β1 |
title_full_unstemmed | MicroRNA-663 regulates the proliferation of fibroblasts in hypertrophic scars via transforming growth factor-β1 |
title_short | MicroRNA-663 regulates the proliferation of fibroblasts in hypertrophic scars via transforming growth factor-β1 |
title_sort | microrna-663 regulates the proliferation of fibroblasts in hypertrophic scars via transforming growth factor-β1 |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6090240/ https://www.ncbi.nlm.nih.gov/pubmed/30116380 http://dx.doi.org/10.3892/etm.2018.6350 |
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