Nogo-A regulates myogenesis via interacting with Filamin-C

Sun Young 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

doi:10.1038/s41420-020-00384-x

Nogo-A regulates myogenesis via interacting with Filamin-C

Sun Young 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 LeeDaehee Hwang, Kyu Shik Jeong

Research output: Contribution to journal › Article › peer-review

6 Scopus citations

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.

Original language	English
Article number	1
Journal	Cell Death Discovery
Volume	7
Issue number	1
DOIs	https://doi.org/10.1038/s41420-020-00384-x
State	Published - Jun 2021

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Park, S. Y., Park, J. H., Kang, U. B., Choi, S. K., Elfadl, A., Ullah, H. M. A., Chung, M. J., Son, J. Y., Yun, H. H., Park, J. M., Yim, J. H., Jung, S. J., Kim, S. H., Choi, Y. C., Kim, D. S., Shin, J. H., Park, J. S., Hur, K., Lee, S. H., ... Jeong, K. S. (2021). Nogo-A regulates myogenesis via interacting with Filamin-C. Cell Death Discovery, 7(1), Article 1. https://doi.org/10.1038/s41420-020-00384-x

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title = "Nogo-A regulates myogenesis via interacting with Filamin-C",

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.",

author = "Park, {Sun Young} and Park, {Ji Hwan} and Kang, {Un Beom} and Choi, {Seong Kyoon} and Ahmed Elfadl and Ullah, {H. M.Arif} and Chung, {Myung Jin} and Son, {Ji Yoon} and Yun, {Hyun Ho} and Park, {Jae Min} and Yim, {Jae hyuk} and Jung, {Seung Jun} and Kim, {Sang Hyup} and Choi, {Young Chul} and Kim, {Dae Seong} and Shin, {Jin Hong} and Park, {Jin Sung} and Keun Hur and Lee, {Sang Han} and Lee, {Eun Joo} and Daehee Hwang and Jeong, {Kyu Shik}",

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month = jun,

doi = "10.1038/s41420-020-00384-x",

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AU - Park, Ji Hwan

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AU - Elfadl, Ahmed

AU - Ullah, H. M.Arif

AU - Chung, Myung Jin

AU - Son, Ji Yoon

AU - Yun, Hyun Ho

AU - Park, Jae Min

AU - Yim, Jae hyuk

AU - Jung, Seung Jun

AU - Kim, Sang Hyup

AU - Choi, Young Chul

AU - Kim, Dae Seong

AU - Shin, Jin Hong

AU - Park, Jin Sung

AU - Hur, Keun

AU - Lee, Sang Han

AU - Lee, Eun Joo

AU - Hwang, Daehee

AU - Jeong, Kyu Shik

PY - 2021/6

Y1 - 2021/6

N2 - 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.

AB - 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.

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Nogo-A regulates myogenesis via interacting with Filamin-C

Abstract

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