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Annexin A1 Deficiency does not Affect Myofiber Repair but Delays Regeneration of Injured Muscles
Repair and regeneration of the injured skeletal myofiber involves fusion of intracellular vesicles with sarcolemma and fusion of the muscle progenitor cells respectively. In vitro experiments have identified involvement of Annexin A1 (Anx A1) in both these fusion processes. To determine if Anx A1 co...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4678367/ https://www.ncbi.nlm.nih.gov/pubmed/26667898 http://dx.doi.org/10.1038/srep18246 |
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author | Leikina, Evgenia Defour, Aurelia Melikov, Kamran Van der Meulen, Jack H. Nagaraju, Kanneboyina Bhuvanendran, Shivaprasad Gebert, Claudia Pfeifer, Karl Chernomordik, Leonid V. Jaiswal, Jyoti K. |
author_facet | Leikina, Evgenia Defour, Aurelia Melikov, Kamran Van der Meulen, Jack H. Nagaraju, Kanneboyina Bhuvanendran, Shivaprasad Gebert, Claudia Pfeifer, Karl Chernomordik, Leonid V. Jaiswal, Jyoti K. |
author_sort | Leikina, Evgenia |
collection | PubMed |
description | Repair and regeneration of the injured skeletal myofiber involves fusion of intracellular vesicles with sarcolemma and fusion of the muscle progenitor cells respectively. In vitro experiments have identified involvement of Annexin A1 (Anx A1) in both these fusion processes. To determine if Anx A1 contributes to these processes during muscle repair in vivo, we have assessed muscle growth and repair in Anx A1-deficient mouse (AnxA1−/−). We found that the lack of Anx A1 does not affect the muscle size and repair of myofibers following focal sarcolemmal injury and lengthening contraction injury. However, the lack of Anx A1 delayed muscle regeneration after notexin-induced injury. This delay in muscle regeneration was not caused by a slowdown in proliferation and differentiation of satellite cells. Instead, lack of Anx A1 lowered the proportion of differentiating myoblasts that managed to fuse with the injured myofibers by days 5 and 7 after notexin injury as compared to the wild type (w.t.) mice. Despite this early slowdown in fusion of Anx A1−/− myoblasts, regeneration caught up at later times post injury. These results establish in vivo role of Anx A1 in cell fusion required for myofiber regeneration and not in intracellular vesicle fusion needed for repair of myofiber sarcolemma. |
format | Online Article Text |
id | pubmed-4678367 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-46783672015-12-18 Annexin A1 Deficiency does not Affect Myofiber Repair but Delays Regeneration of Injured Muscles Leikina, Evgenia Defour, Aurelia Melikov, Kamran Van der Meulen, Jack H. Nagaraju, Kanneboyina Bhuvanendran, Shivaprasad Gebert, Claudia Pfeifer, Karl Chernomordik, Leonid V. Jaiswal, Jyoti K. Sci Rep Article Repair and regeneration of the injured skeletal myofiber involves fusion of intracellular vesicles with sarcolemma and fusion of the muscle progenitor cells respectively. In vitro experiments have identified involvement of Annexin A1 (Anx A1) in both these fusion processes. To determine if Anx A1 contributes to these processes during muscle repair in vivo, we have assessed muscle growth and repair in Anx A1-deficient mouse (AnxA1−/−). We found that the lack of Anx A1 does not affect the muscle size and repair of myofibers following focal sarcolemmal injury and lengthening contraction injury. However, the lack of Anx A1 delayed muscle regeneration after notexin-induced injury. This delay in muscle regeneration was not caused by a slowdown in proliferation and differentiation of satellite cells. Instead, lack of Anx A1 lowered the proportion of differentiating myoblasts that managed to fuse with the injured myofibers by days 5 and 7 after notexin injury as compared to the wild type (w.t.) mice. Despite this early slowdown in fusion of Anx A1−/− myoblasts, regeneration caught up at later times post injury. These results establish in vivo role of Anx A1 in cell fusion required for myofiber regeneration and not in intracellular vesicle fusion needed for repair of myofiber sarcolemma. Nature Publishing Group 2015-12-15 /pmc/articles/PMC4678367/ /pubmed/26667898 http://dx.doi.org/10.1038/srep18246 Text en Copyright © 2015, 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 Leikina, Evgenia Defour, Aurelia Melikov, Kamran Van der Meulen, Jack H. Nagaraju, Kanneboyina Bhuvanendran, Shivaprasad Gebert, Claudia Pfeifer, Karl Chernomordik, Leonid V. Jaiswal, Jyoti K. Annexin A1 Deficiency does not Affect Myofiber Repair but Delays Regeneration of Injured Muscles |
title | Annexin A1 Deficiency does not Affect Myofiber Repair but Delays Regeneration of Injured Muscles |
title_full | Annexin A1 Deficiency does not Affect Myofiber Repair but Delays Regeneration of Injured Muscles |
title_fullStr | Annexin A1 Deficiency does not Affect Myofiber Repair but Delays Regeneration of Injured Muscles |
title_full_unstemmed | Annexin A1 Deficiency does not Affect Myofiber Repair but Delays Regeneration of Injured Muscles |
title_short | Annexin A1 Deficiency does not Affect Myofiber Repair but Delays Regeneration of Injured Muscles |
title_sort | annexin a1 deficiency does not affect myofiber repair but delays regeneration of injured muscles |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4678367/ https://www.ncbi.nlm.nih.gov/pubmed/26667898 http://dx.doi.org/10.1038/srep18246 |
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