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REAC technology and hyaluron synthase 2, an interesting network to slow down stem cell senescence
Hyaluronic acid (HA) plays a fundamental role in cell polarity and hydrodynamic processes, affording significant modulation of proliferation, migration, morphogenesis and senescence, with deep implication in the ability of stem cells to execute their differentiating plans. The Radio Electric Asymmet...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4919615/ https://www.ncbi.nlm.nih.gov/pubmed/27339908 http://dx.doi.org/10.1038/srep28682 |
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author | Maioli, Margherita Rinaldi, Salvatore Pigliaru, Gianfranco Santaniello, Sara Basoli, Valentina Castagna, Alessandro Fontani, Vania Ventura, Carlo |
author_facet | Maioli, Margherita Rinaldi, Salvatore Pigliaru, Gianfranco Santaniello, Sara Basoli, Valentina Castagna, Alessandro Fontani, Vania Ventura, Carlo |
author_sort | Maioli, Margherita |
collection | PubMed |
description | Hyaluronic acid (HA) plays a fundamental role in cell polarity and hydrodynamic processes, affording significant modulation of proliferation, migration, morphogenesis and senescence, with deep implication in the ability of stem cells to execute their differentiating plans. The Radio Electric Asymmetric Conveyer (REAC) technology is aimed to optimize the ions fluxes at the molecular level in order to optimize the molecular mechanisms driving cellular asymmetry and polarization. Here, we show that treatment with 4-methylumbelliferone (4-MU), a potent repressor of type 2 HA synthase and endogenous HA synthesis, dramatically antagonized the ability of REAC to recover the gene and protein expression of Bmi1, Oct4, Sox2, and Nanog in ADhMSCs that had been made senescent by prolonged culture up to the 30(th) passage. In senescent ADhMSCs, 4-MU also counteracted the REAC ability to rescue the gene expression of TERT, and the associated resumption of telomerase activity. Hence, the anti-senescence action of REAC is largely dependent upon the availability of endogenous HA synthesis. Endogenous HA and HA-binding proteins with REAC technology create an interesting network that acts on the modulation of cell polarity and intracellular environment. This suggests that REAC technology is effective on an intracellular niche level of stem cell regulation. |
format | Online Article Text |
id | pubmed-4919615 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-49196152016-06-28 REAC technology and hyaluron synthase 2, an interesting network to slow down stem cell senescence Maioli, Margherita Rinaldi, Salvatore Pigliaru, Gianfranco Santaniello, Sara Basoli, Valentina Castagna, Alessandro Fontani, Vania Ventura, Carlo Sci Rep Article Hyaluronic acid (HA) plays a fundamental role in cell polarity and hydrodynamic processes, affording significant modulation of proliferation, migration, morphogenesis and senescence, with deep implication in the ability of stem cells to execute their differentiating plans. The Radio Electric Asymmetric Conveyer (REAC) technology is aimed to optimize the ions fluxes at the molecular level in order to optimize the molecular mechanisms driving cellular asymmetry and polarization. Here, we show that treatment with 4-methylumbelliferone (4-MU), a potent repressor of type 2 HA synthase and endogenous HA synthesis, dramatically antagonized the ability of REAC to recover the gene and protein expression of Bmi1, Oct4, Sox2, and Nanog in ADhMSCs that had been made senescent by prolonged culture up to the 30(th) passage. In senescent ADhMSCs, 4-MU also counteracted the REAC ability to rescue the gene expression of TERT, and the associated resumption of telomerase activity. Hence, the anti-senescence action of REAC is largely dependent upon the availability of endogenous HA synthesis. Endogenous HA and HA-binding proteins with REAC technology create an interesting network that acts on the modulation of cell polarity and intracellular environment. This suggests that REAC technology is effective on an intracellular niche level of stem cell regulation. Nature Publishing Group 2016-06-24 /pmc/articles/PMC4919615/ /pubmed/27339908 http://dx.doi.org/10.1038/srep28682 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Maioli, Margherita Rinaldi, Salvatore Pigliaru, Gianfranco Santaniello, Sara Basoli, Valentina Castagna, Alessandro Fontani, Vania Ventura, Carlo REAC technology and hyaluron synthase 2, an interesting network to slow down stem cell senescence |
title | REAC technology and hyaluron synthase 2, an interesting network to slow down stem cell senescence |
title_full | REAC technology and hyaluron synthase 2, an interesting network to slow down stem cell senescence |
title_fullStr | REAC technology and hyaluron synthase 2, an interesting network to slow down stem cell senescence |
title_full_unstemmed | REAC technology and hyaluron synthase 2, an interesting network to slow down stem cell senescence |
title_short | REAC technology and hyaluron synthase 2, an interesting network to slow down stem cell senescence |
title_sort | reac technology and hyaluron synthase 2, an interesting network to slow down stem cell senescence |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4919615/ https://www.ncbi.nlm.nih.gov/pubmed/27339908 http://dx.doi.org/10.1038/srep28682 |
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