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Inhibiting function of human fetal dermal mesenchymal stem cells on bioactivities of keloid fibroblasts
BACKGROUND: Keloid is one kind of benign skin disease caused by hyperplasia of fibroblasts and collagen fibrils. It is refractory due to the lack of an effective treatment at present, which puts pressure on seeking a new therapeutic regimen. Mesenchymal stem cells (MSCs) from fetal skin are consider...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5516368/ https://www.ncbi.nlm.nih.gov/pubmed/28720118 http://dx.doi.org/10.1186/s13287-017-0624-0 |
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author | Jiao, Ya Wang, Xiao Zhang, Jixun Qi, Yongjun Gong, Hongmin Jiang, Duyin |
author_facet | Jiao, Ya Wang, Xiao Zhang, Jixun Qi, Yongjun Gong, Hongmin Jiang, Duyin |
author_sort | Jiao, Ya |
collection | PubMed |
description | BACKGROUND: Keloid is one kind of benign skin disease caused by hyperplasia of fibroblasts and collagen fibrils. It is refractory due to the lack of an effective treatment at present, which puts pressure on seeking a new therapeutic regimen. Mesenchymal stem cells (MSCs) from fetal skin are considered to play a crucial role in scarless healing. Nevertheless, the efficacy of them in keloid disorders remains poorly understood. METHODS: Keloid fibroblasts (KFs), human adult dermal fibroblasts (ADFs), and human fetal dermal mesenchymal stem cells (FDMSCs) were isolated to single cells and cultured in Dulbecco’s modified Eagle’s medium (DMEM). ADFs and FDMSCs were used to generate ADF-conditioned medium (A-CM) and FDMSC-conditioned medium (F-CM). The effects of A-CM and F-CM on KFs were tested using MTT assay, BrdU assay, TUNEL assay, quantitative polymerase chain reaction, Western blot, and annexin V-FITC/PI binding assay,. RESULTS: FDMSCs inhibited the bioactivity of KFs, downregulated the expression of the antiapoptotic protein BCL-2, and upregulated the expression of the proapoptotic protein BAX of KFs by secreting some soluble substances, thus accelerating the apoptosis of KFs. CONCLUSION: F-CM induces apoptosis of KFs, providing a novel treatment strategy for keloid disorders. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13287-017-0624-0) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-5516368 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-55163682017-07-20 Inhibiting function of human fetal dermal mesenchymal stem cells on bioactivities of keloid fibroblasts Jiao, Ya Wang, Xiao Zhang, Jixun Qi, Yongjun Gong, Hongmin Jiang, Duyin Stem Cell Res Ther Short Report BACKGROUND: Keloid is one kind of benign skin disease caused by hyperplasia of fibroblasts and collagen fibrils. It is refractory due to the lack of an effective treatment at present, which puts pressure on seeking a new therapeutic regimen. Mesenchymal stem cells (MSCs) from fetal skin are considered to play a crucial role in scarless healing. Nevertheless, the efficacy of them in keloid disorders remains poorly understood. METHODS: Keloid fibroblasts (KFs), human adult dermal fibroblasts (ADFs), and human fetal dermal mesenchymal stem cells (FDMSCs) were isolated to single cells and cultured in Dulbecco’s modified Eagle’s medium (DMEM). ADFs and FDMSCs were used to generate ADF-conditioned medium (A-CM) and FDMSC-conditioned medium (F-CM). The effects of A-CM and F-CM on KFs were tested using MTT assay, BrdU assay, TUNEL assay, quantitative polymerase chain reaction, Western blot, and annexin V-FITC/PI binding assay,. RESULTS: FDMSCs inhibited the bioactivity of KFs, downregulated the expression of the antiapoptotic protein BCL-2, and upregulated the expression of the proapoptotic protein BAX of KFs by secreting some soluble substances, thus accelerating the apoptosis of KFs. CONCLUSION: F-CM induces apoptosis of KFs, providing a novel treatment strategy for keloid disorders. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13287-017-0624-0) contains supplementary material, which is available to authorized users. BioMed Central 2017-07-18 /pmc/articles/PMC5516368/ /pubmed/28720118 http://dx.doi.org/10.1186/s13287-017-0624-0 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Short Report Jiao, Ya Wang, Xiao Zhang, Jixun Qi, Yongjun Gong, Hongmin Jiang, Duyin Inhibiting function of human fetal dermal mesenchymal stem cells on bioactivities of keloid fibroblasts |
title | Inhibiting function of human fetal dermal mesenchymal stem cells on bioactivities of keloid fibroblasts |
title_full | Inhibiting function of human fetal dermal mesenchymal stem cells on bioactivities of keloid fibroblasts |
title_fullStr | Inhibiting function of human fetal dermal mesenchymal stem cells on bioactivities of keloid fibroblasts |
title_full_unstemmed | Inhibiting function of human fetal dermal mesenchymal stem cells on bioactivities of keloid fibroblasts |
title_short | Inhibiting function of human fetal dermal mesenchymal stem cells on bioactivities of keloid fibroblasts |
title_sort | inhibiting function of human fetal dermal mesenchymal stem cells on bioactivities of keloid fibroblasts |
topic | Short Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5516368/ https://www.ncbi.nlm.nih.gov/pubmed/28720118 http://dx.doi.org/10.1186/s13287-017-0624-0 |
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