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Loss of niche-satellite cell interactions in syndecan-3 null mice alters muscle progenitor cell homeostasis improving muscle regeneration
BACKGROUND: The skeletal muscle stem cell niche provides an environment that maintains quiescent satellite cells, required for skeletal muscle homeostasis and regeneration. Syndecan-3, a transmembrane proteoglycan expressed in satellite cells, supports communication with the niche, providing cell in...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5064903/ https://www.ncbi.nlm.nih.gov/pubmed/27757223 http://dx.doi.org/10.1186/s13395-016-0104-8 |
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author | Pisconti, Addolorata Banks, Glen B. Babaeijandaghi, Farshad Betta, Nicole Dalla Rossi, Fabio M. V. Chamberlain, Jeffrey S. Olwin, Bradley B. |
author_facet | Pisconti, Addolorata Banks, Glen B. Babaeijandaghi, Farshad Betta, Nicole Dalla Rossi, Fabio M. V. Chamberlain, Jeffrey S. Olwin, Bradley B. |
author_sort | Pisconti, Addolorata |
collection | PubMed |
description | BACKGROUND: The skeletal muscle stem cell niche provides an environment that maintains quiescent satellite cells, required for skeletal muscle homeostasis and regeneration. Syndecan-3, a transmembrane proteoglycan expressed in satellite cells, supports communication with the niche, providing cell interactions and signals to maintain quiescent satellite cells. RESULTS: Syndecan-3 ablation unexpectedly improves regeneration in repeatedly injured muscle and in dystrophic mice, accompanied by the persistence of sublaminar and interstitial, proliferating myoblasts. Additionally, muscle aging is improved in syndecan-3 null mice. Since syndecan-3 null myofiber-associated satellite cells downregulate Pax7 and migrate away from the niche more readily than wild type cells, syxndecan-3 appears to regulate satellite cell homeostasis and satellite cell homing to the niche. CONCLUSIONS: Manipulating syndecan-3 provides a promising target for development of therapies to enhance muscle regeneration in muscular dystrophies and in aged muscle. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13395-016-0104-8) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-5064903 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-50649032016-10-18 Loss of niche-satellite cell interactions in syndecan-3 null mice alters muscle progenitor cell homeostasis improving muscle regeneration Pisconti, Addolorata Banks, Glen B. Babaeijandaghi, Farshad Betta, Nicole Dalla Rossi, Fabio M. V. Chamberlain, Jeffrey S. Olwin, Bradley B. Skelet Muscle Research BACKGROUND: The skeletal muscle stem cell niche provides an environment that maintains quiescent satellite cells, required for skeletal muscle homeostasis and regeneration. Syndecan-3, a transmembrane proteoglycan expressed in satellite cells, supports communication with the niche, providing cell interactions and signals to maintain quiescent satellite cells. RESULTS: Syndecan-3 ablation unexpectedly improves regeneration in repeatedly injured muscle and in dystrophic mice, accompanied by the persistence of sublaminar and interstitial, proliferating myoblasts. Additionally, muscle aging is improved in syndecan-3 null mice. Since syndecan-3 null myofiber-associated satellite cells downregulate Pax7 and migrate away from the niche more readily than wild type cells, syxndecan-3 appears to regulate satellite cell homeostasis and satellite cell homing to the niche. CONCLUSIONS: Manipulating syndecan-3 provides a promising target for development of therapies to enhance muscle regeneration in muscular dystrophies and in aged muscle. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13395-016-0104-8) contains supplementary material, which is available to authorized users. BioMed Central 2016-10-04 /pmc/articles/PMC5064903/ /pubmed/27757223 http://dx.doi.org/10.1186/s13395-016-0104-8 Text en © The Author(s). 2016 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 Pisconti, Addolorata Banks, Glen B. Babaeijandaghi, Farshad Betta, Nicole Dalla Rossi, Fabio M. V. Chamberlain, Jeffrey S. Olwin, Bradley B. Loss of niche-satellite cell interactions in syndecan-3 null mice alters muscle progenitor cell homeostasis improving muscle regeneration |
title | Loss of niche-satellite cell interactions in syndecan-3 null mice alters muscle progenitor cell homeostasis improving muscle regeneration |
title_full | Loss of niche-satellite cell interactions in syndecan-3 null mice alters muscle progenitor cell homeostasis improving muscle regeneration |
title_fullStr | Loss of niche-satellite cell interactions in syndecan-3 null mice alters muscle progenitor cell homeostasis improving muscle regeneration |
title_full_unstemmed | Loss of niche-satellite cell interactions in syndecan-3 null mice alters muscle progenitor cell homeostasis improving muscle regeneration |
title_short | Loss of niche-satellite cell interactions in syndecan-3 null mice alters muscle progenitor cell homeostasis improving muscle regeneration |
title_sort | loss of niche-satellite cell interactions in syndecan-3 null mice alters muscle progenitor cell homeostasis improving muscle regeneration |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5064903/ https://www.ncbi.nlm.nih.gov/pubmed/27757223 http://dx.doi.org/10.1186/s13395-016-0104-8 |
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