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Activation of skeletal muscle–resident glial cells upon nerve injury
Here, we report on the identification of Itga7-expressing muscle-resident glial cells activated by loss of neuromuscular junction (NMJ) integrity. Gene expression analysis at the bulk and single-cell level revealed that these cells are distinct from Itga7-expressing muscle satellite cells. We show t...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Society for Clinical Investigation
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8119188/ https://www.ncbi.nlm.nih.gov/pubmed/33661767 http://dx.doi.org/10.1172/jci.insight.143469 |
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author | Proietti, Daisy Giordani, Lorenzo De Bardi, Marco D’Ercole, Chiara Lozanoska-Ochser, Biliana Amadio, Susanna Volonté, Cinzia Marinelli, Sara Muchir, Antoine Bouché, Marina Borsellino, Giovanna Sacco, Alessandra Puri, Pier Lorenzo Madaro, Luca |
author_facet | Proietti, Daisy Giordani, Lorenzo De Bardi, Marco D’Ercole, Chiara Lozanoska-Ochser, Biliana Amadio, Susanna Volonté, Cinzia Marinelli, Sara Muchir, Antoine Bouché, Marina Borsellino, Giovanna Sacco, Alessandra Puri, Pier Lorenzo Madaro, Luca |
author_sort | Proietti, Daisy |
collection | PubMed |
description | Here, we report on the identification of Itga7-expressing muscle-resident glial cells activated by loss of neuromuscular junction (NMJ) integrity. Gene expression analysis at the bulk and single-cell level revealed that these cells are distinct from Itga7-expressing muscle satellite cells. We show that a selective activation and expansion of Itga7(+) glial cells occur in response to muscle nerve lesion. Upon activation, muscle glial–derived progenies expressed neurotrophic genes, including nerve growth factor receptor, which enables their isolation by FACS. We show that activated muscle glial cells also expressed genes potentially implicated in extracellular matrix remodeling at NMJs. We found that tenascin C, which was highly expressed by muscle glial cells, activated upon nerve injury and preferentially localized to NMJ. Interestingly, we observed that the activation of muscle glial cells by acute nerve injury was reversible upon NMJ repair. By contrast, in a mouse model of ALS, in which NMJ degeneration is progressive, muscle glial cells steadily increased over the course of the disease. However, they exhibited an impaired neurotrophic activity, suggesting that pathogenic activation of glial cells may be implicated in ALS progression. |
format | Online Article Text |
id | pubmed-8119188 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | American Society for Clinical Investigation |
record_format | MEDLINE/PubMed |
spelling | pubmed-81191882021-05-18 Activation of skeletal muscle–resident glial cells upon nerve injury Proietti, Daisy Giordani, Lorenzo De Bardi, Marco D’Ercole, Chiara Lozanoska-Ochser, Biliana Amadio, Susanna Volonté, Cinzia Marinelli, Sara Muchir, Antoine Bouché, Marina Borsellino, Giovanna Sacco, Alessandra Puri, Pier Lorenzo Madaro, Luca JCI Insight Research Article Here, we report on the identification of Itga7-expressing muscle-resident glial cells activated by loss of neuromuscular junction (NMJ) integrity. Gene expression analysis at the bulk and single-cell level revealed that these cells are distinct from Itga7-expressing muscle satellite cells. We show that a selective activation and expansion of Itga7(+) glial cells occur in response to muscle nerve lesion. Upon activation, muscle glial–derived progenies expressed neurotrophic genes, including nerve growth factor receptor, which enables their isolation by FACS. We show that activated muscle glial cells also expressed genes potentially implicated in extracellular matrix remodeling at NMJs. We found that tenascin C, which was highly expressed by muscle glial cells, activated upon nerve injury and preferentially localized to NMJ. Interestingly, we observed that the activation of muscle glial cells by acute nerve injury was reversible upon NMJ repair. By contrast, in a mouse model of ALS, in which NMJ degeneration is progressive, muscle glial cells steadily increased over the course of the disease. However, they exhibited an impaired neurotrophic activity, suggesting that pathogenic activation of glial cells may be implicated in ALS progression. American Society for Clinical Investigation 2021-04-08 /pmc/articles/PMC8119188/ /pubmed/33661767 http://dx.doi.org/10.1172/jci.insight.143469 Text en © 2021 Proietti et al. https://creativecommons.org/licenses/by/4.0/This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Research Article Proietti, Daisy Giordani, Lorenzo De Bardi, Marco D’Ercole, Chiara Lozanoska-Ochser, Biliana Amadio, Susanna Volonté, Cinzia Marinelli, Sara Muchir, Antoine Bouché, Marina Borsellino, Giovanna Sacco, Alessandra Puri, Pier Lorenzo Madaro, Luca Activation of skeletal muscle–resident glial cells upon nerve injury |
title | Activation of skeletal muscle–resident glial cells upon nerve injury |
title_full | Activation of skeletal muscle–resident glial cells upon nerve injury |
title_fullStr | Activation of skeletal muscle–resident glial cells upon nerve injury |
title_full_unstemmed | Activation of skeletal muscle–resident glial cells upon nerve injury |
title_short | Activation of skeletal muscle–resident glial cells upon nerve injury |
title_sort | activation of skeletal muscle–resident glial cells upon nerve injury |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8119188/ https://www.ncbi.nlm.nih.gov/pubmed/33661767 http://dx.doi.org/10.1172/jci.insight.143469 |
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