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Inhibition of class I HDACs preserves hair follicle inductivity in postnatal dermal cells
Induction of new hair follicles (HFs) may be an ultimate treatment goal for alopecia; however, functional cells with HF inductivity must be expanded in bulk for clinical use. In vitro culture conditions are completely different from the in vivo microenvironment. Although fetal and postnatal dermal c...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8674223/ https://www.ncbi.nlm.nih.gov/pubmed/34911993 http://dx.doi.org/10.1038/s41598-021-03508-0 |
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author | Park, Minji Jang, Sunhyae Chung, Jin Ho Kwon, Ohsang Jo, Seong Jin |
author_facet | Park, Minji Jang, Sunhyae Chung, Jin Ho Kwon, Ohsang Jo, Seong Jin |
author_sort | Park, Minji |
collection | PubMed |
description | Induction of new hair follicles (HFs) may be an ultimate treatment goal for alopecia; however, functional cells with HF inductivity must be expanded in bulk for clinical use. In vitro culture conditions are completely different from the in vivo microenvironment. Although fetal and postnatal dermal cells (DCs) have the potential to induce HFs, they rapidly lose this HF inductivity during culture, accompanied by a drastic change in gene expression. This suggests that epigenetic regulation may be involved. Of the various histone deacetylases (HDACs), Class I HDACs are noteworthy because they are ubiquitously expressed and have the strongest deacetylase activity. This study revealed that DCs from postnatal mice rapidly lose HF inductivity and that this reduction is accompanied by a significant decrease in histone H3 acetylation. However, MS-275, an inhibitor of class I HDACs, preserves HF inductivity in DCs during culture, increasing alkaline phosphatase activity and upregulating HF inductive genes such as BMP4, HEY1, and WIF1. In addition, the inhibition of class I HDACs activates the Wnt signaling pathway, the most well-described molecular pathway in HF development, via increased histone H3 acetylation within the promoter region of the Wnt transcription factor LEF1. Our results suggest that class I HDACs could be a potential target for the neogenesis of HFs. |
format | Online Article Text |
id | pubmed-8674223 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-86742232021-12-16 Inhibition of class I HDACs preserves hair follicle inductivity in postnatal dermal cells Park, Minji Jang, Sunhyae Chung, Jin Ho Kwon, Ohsang Jo, Seong Jin Sci Rep Article Induction of new hair follicles (HFs) may be an ultimate treatment goal for alopecia; however, functional cells with HF inductivity must be expanded in bulk for clinical use. In vitro culture conditions are completely different from the in vivo microenvironment. Although fetal and postnatal dermal cells (DCs) have the potential to induce HFs, they rapidly lose this HF inductivity during culture, accompanied by a drastic change in gene expression. This suggests that epigenetic regulation may be involved. Of the various histone deacetylases (HDACs), Class I HDACs are noteworthy because they are ubiquitously expressed and have the strongest deacetylase activity. This study revealed that DCs from postnatal mice rapidly lose HF inductivity and that this reduction is accompanied by a significant decrease in histone H3 acetylation. However, MS-275, an inhibitor of class I HDACs, preserves HF inductivity in DCs during culture, increasing alkaline phosphatase activity and upregulating HF inductive genes such as BMP4, HEY1, and WIF1. In addition, the inhibition of class I HDACs activates the Wnt signaling pathway, the most well-described molecular pathway in HF development, via increased histone H3 acetylation within the promoter region of the Wnt transcription factor LEF1. Our results suggest that class I HDACs could be a potential target for the neogenesis of HFs. Nature Publishing Group UK 2021-12-15 /pmc/articles/PMC8674223/ /pubmed/34911993 http://dx.doi.org/10.1038/s41598-021-03508-0 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Park, Minji Jang, Sunhyae Chung, Jin Ho Kwon, Ohsang Jo, Seong Jin Inhibition of class I HDACs preserves hair follicle inductivity in postnatal dermal cells |
title | Inhibition of class I HDACs preserves hair follicle inductivity in postnatal dermal cells |
title_full | Inhibition of class I HDACs preserves hair follicle inductivity in postnatal dermal cells |
title_fullStr | Inhibition of class I HDACs preserves hair follicle inductivity in postnatal dermal cells |
title_full_unstemmed | Inhibition of class I HDACs preserves hair follicle inductivity in postnatal dermal cells |
title_short | Inhibition of class I HDACs preserves hair follicle inductivity in postnatal dermal cells |
title_sort | inhibition of class i hdacs preserves hair follicle inductivity in postnatal dermal cells |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8674223/ https://www.ncbi.nlm.nih.gov/pubmed/34911993 http://dx.doi.org/10.1038/s41598-021-03508-0 |
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