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Antioxidants inhibit cell senescence and preserve stemness of adipose tissue-derived stem cells by reducing ROS generation during long-term in vitro expansion
BACKGROUND: Adipose tissue-derived mesenchymal stem cells (ADSCs) are promising candidates for regenerative medicine. However, long-term in vitro passaging leads to stemness loss and cell senescence of ADSCs, resulting in failure of ADSC-based therapy. METHODS: In this study, ADSCs were treated with...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6798439/ https://www.ncbi.nlm.nih.gov/pubmed/31623678 http://dx.doi.org/10.1186/s13287-019-1404-9 |
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author | Liao, Naishun Shi, Yingjun Zhang, Cuilin Zheng, Youshi Wang, Yingchao Zhao, Bixing Zeng, Yongyi Liu, Xiaolong Liu, Jingfeng |
author_facet | Liao, Naishun Shi, Yingjun Zhang, Cuilin Zheng, Youshi Wang, Yingchao Zhao, Bixing Zeng, Yongyi Liu, Xiaolong Liu, Jingfeng |
author_sort | Liao, Naishun |
collection | PubMed |
description | BACKGROUND: Adipose tissue-derived mesenchymal stem cells (ADSCs) are promising candidates for regenerative medicine. However, long-term in vitro passaging leads to stemness loss and cell senescence of ADSCs, resulting in failure of ADSC-based therapy. METHODS: In this study, ADSCs were treated with low dose of antioxidants (reduced glutathione and melatonin) with anti-aging and stem cell protection properties in the in vitro passaging, and the cell functions including stem cell senescence, cell migration, cell multidirectional differentiation potential, and ROS content were carefully analyzed. RESULTS: We found that GSH and melatonin could maintain ADSC cell functions through reducing cell senescence and promoting cell migration, as well as by preserving stemness and multidirectional differentiation potential, through inhibiting ROS generation during long-term expansion of ADSCs. CONCLUSIONS: Our results suggested that antioxidant treatment could efficiently prevent the dysfunction and preserve cell functions of ADSCs after long-term passaging, providing a practical strategy to facilitate ADSC-based therapy. |
format | Online Article Text |
id | pubmed-6798439 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-67984392019-10-21 Antioxidants inhibit cell senescence and preserve stemness of adipose tissue-derived stem cells by reducing ROS generation during long-term in vitro expansion Liao, Naishun Shi, Yingjun Zhang, Cuilin Zheng, Youshi Wang, Yingchao Zhao, Bixing Zeng, Yongyi Liu, Xiaolong Liu, Jingfeng Stem Cell Res Ther Research BACKGROUND: Adipose tissue-derived mesenchymal stem cells (ADSCs) are promising candidates for regenerative medicine. However, long-term in vitro passaging leads to stemness loss and cell senescence of ADSCs, resulting in failure of ADSC-based therapy. METHODS: In this study, ADSCs were treated with low dose of antioxidants (reduced glutathione and melatonin) with anti-aging and stem cell protection properties in the in vitro passaging, and the cell functions including stem cell senescence, cell migration, cell multidirectional differentiation potential, and ROS content were carefully analyzed. RESULTS: We found that GSH and melatonin could maintain ADSC cell functions through reducing cell senescence and promoting cell migration, as well as by preserving stemness and multidirectional differentiation potential, through inhibiting ROS generation during long-term expansion of ADSCs. CONCLUSIONS: Our results suggested that antioxidant treatment could efficiently prevent the dysfunction and preserve cell functions of ADSCs after long-term passaging, providing a practical strategy to facilitate ADSC-based therapy. BioMed Central 2019-10-17 /pmc/articles/PMC6798439/ /pubmed/31623678 http://dx.doi.org/10.1186/s13287-019-1404-9 Text en © The Author(s). 2019 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 | Research Liao, Naishun Shi, Yingjun Zhang, Cuilin Zheng, Youshi Wang, Yingchao Zhao, Bixing Zeng, Yongyi Liu, Xiaolong Liu, Jingfeng Antioxidants inhibit cell senescence and preserve stemness of adipose tissue-derived stem cells by reducing ROS generation during long-term in vitro expansion |
title | Antioxidants inhibit cell senescence and preserve stemness of adipose tissue-derived stem cells by reducing ROS generation during long-term in vitro expansion |
title_full | Antioxidants inhibit cell senescence and preserve stemness of adipose tissue-derived stem cells by reducing ROS generation during long-term in vitro expansion |
title_fullStr | Antioxidants inhibit cell senescence and preserve stemness of adipose tissue-derived stem cells by reducing ROS generation during long-term in vitro expansion |
title_full_unstemmed | Antioxidants inhibit cell senescence and preserve stemness of adipose tissue-derived stem cells by reducing ROS generation during long-term in vitro expansion |
title_short | Antioxidants inhibit cell senescence and preserve stemness of adipose tissue-derived stem cells by reducing ROS generation during long-term in vitro expansion |
title_sort | antioxidants inhibit cell senescence and preserve stemness of adipose tissue-derived stem cells by reducing ros generation during long-term in vitro expansion |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6798439/ https://www.ncbi.nlm.nih.gov/pubmed/31623678 http://dx.doi.org/10.1186/s13287-019-1404-9 |
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