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Nogo-A regulates myogenesis via interacting with Filamin-C

Authors
 SunYoung Park  ;  Ji-Hwan Park  ;  Un-Beom Kang  ;  Seong-Kyoon Choi  ;  Ahmed Elfadl  ;  H M Arif Ullah  ;  Myung-Jin Chung  ;  Ji-Yoon Son  ;  Hyun Ho Yun  ;  Jae-Min Park  ;  Jae-Hyuk Yim  ;  Seung-Jun Jung  ;  Sang-Hyup Kim  ;  Young-Chul Choi  ;  Dae-Seong Kim  ;  Jin-Hong Shin  ;  Jin-Sung Park  ;  Keun Hur  ;  Sang-Han Lee  ;  Eun-Joo Lee  ;  Daehee Hwang  ;  Kyu-Shik Jeong 
Citation
 CELL DEATH DISCOVERY, Vol.7(1), 2021-01 
Journal Title
 CELL DEATH DISCOVERY 
Issue Date
2021-01
Abstract
Among the three isoforms encoded by Rtn4, Nogo-A has been intensely investigated as a central nervous system inhibitor. Although Nogo-A expression is increased in muscles of patients with amyotrophic lateral sclerosis, its role in muscle homeostasis and regeneration is not well elucidated. In this study, we discovered a significant increase in Nogo-A expression in various muscle-related pathological conditions. Nogo-/- mice displayed dystrophic muscle structure, dysregulated muscle regeneration following injury, and altered gene expression involving lipid storage and muscle cell differentiation. We hypothesized that increased Nogo-A levels might regulate muscle regeneration. Differentiating myoblasts exhibited Nogo-A upregulation and silencing Nogo-A abrogated myoblast differentiation. Nogo-A interacted with filamin-C, suggesting a role for Nogo-A in cytoskeletal arrangement during myogenesis. In conclusion, Nogo-A maintains muscle homeostasis and integrity, and pathologically altered Nogo-A expression mediates muscle regeneration, suggesting Nogo-A as a novel target for the treatment of myopathies in clinical settings.
Files in This Item:
T202100884.pdf Download
DOI
10.1038/s41420-020-00384-x
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers
Yonsei Authors
Choi, Young Chul(최영철) ORCID logo https://orcid.org/0000-0001-5525-6861
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/182272
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