G-CSF supports long-term muscle regeneration in mouse models of muscular dystrophy

Nozomi Hayashiji; Shinsuke Yuasa; Yuko Miyagoe-Suzuki; Mie Hara; Naoki Ito; Hisayuki Hashimoto; Dai Kusumoto; Tomohisa Seki; Shugo Tohyama; Masaki Kodaira; Akira Kunitomi; Shin Kashimura; Makoto Takei; Yuki Saito; Shinichiro Okata; Toru Egashira; Jin Endo; Toshikuni Sasaoka; Shin'ichi Takeda; Keiichi Fukuda

doi:10.1038/ncomms7745

G-CSF supports long-term muscle regeneration in mouse models of muscular dystrophy

Nozomi Hayashiji, Shinsuke Yuasa, Yuko Miyagoe-Suzuki, Mie Hara, Naoki Ito, Hisayuki Hashimoto, Dai Kusumoto, Tomohisa Seki, Shugo Tohyama, Masaki Kodaira, Akira Kunitomi, Shin Kashimura, Makoto Takei, Yuki Saito, Shinichiro Okata, Toru Egashira, Jin Endo, Toshikuni Sasaoka, Shin'ichi Takeda, Keiichi Fukuda

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

36 Citations (Scopus)

Abstract

Duchenne muscular dystrophy (DMD) is a chronic and life-threatening disease that is initially supported by muscle regeneration but eventually shows satellite cell exhaustion and muscular dysfunction. The life-long maintenance of skeletal muscle homoeostasis requires the satellite stem cell pool to be preserved. Asymmetric cell division plays a pivotal role in the maintenance of the satellite cell pool. Here we show that granulocyte colony-stimulating factor receptor (G-CSFR) is asymmetrically expressed in activated satellite cells. G-CSF positively affects the satellite cell population during multiple stages of differentiation in ex vivo cultured fibres. G-CSF could be important in developing an effective therapy for DMD based on its potential to modulate the supply of multiple stages of regenerated myocytes. This study shows that the G-CSF-G-CSFR axis is fundamentally important for long-term muscle regeneration, functional maintenance and lifespan extension in mouse models of DMD with varying severities.

Original language	English
Article number	6745
Journal	Nature communications
Volume	6
DOIs	https://doi.org/10.1038/ncomms7745
Publication status	Published - 2015 Apr 13

ASJC Scopus subject areas

Chemistry(all)
Biochemistry, Genetics and Molecular Biology(all)
Physics and Astronomy(all)

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Hayashiji, N., Yuasa, S., Miyagoe-Suzuki, Y., Hara, M., Ito, N., Hashimoto, H., Kusumoto, D., Seki, T., Tohyama, S., Kodaira, M., Kunitomi, A., Kashimura, S., Takei, M., Saito, Y., Okata, S., Egashira, T., Endo, J., Sasaoka, T., Takeda, S., & Fukuda, K. (2015). G-CSF supports long-term muscle regeneration in mouse models of muscular dystrophy. Nature communications, 6, Article 6745. https://doi.org/10.1038/ncomms7745

Hayashiji, N, Yuasa, S, Miyagoe-Suzuki, Y, Hara, M, Ito, N, Hashimoto, H, Kusumoto, D, Seki, T, Tohyama, S, Kodaira, M, Kunitomi, A, Kashimura, S, Takei, M, Saito, Y, Okata, S, Egashira, T, Endo, J, Sasaoka, T, Takeda, S & Fukuda, K 2015, 'G-CSF supports long-term muscle regeneration in mouse models of muscular dystrophy', Nature communications, vol. 6, 6745. https://doi.org/10.1038/ncomms7745

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title = "G-CSF supports long-term muscle regeneration in mouse models of muscular dystrophy",

abstract = "Duchenne muscular dystrophy (DMD) is a chronic and life-threatening disease that is initially supported by muscle regeneration but eventually shows satellite cell exhaustion and muscular dysfunction. The life-long maintenance of skeletal muscle homoeostasis requires the satellite stem cell pool to be preserved. Asymmetric cell division plays a pivotal role in the maintenance of the satellite cell pool. Here we show that granulocyte colony-stimulating factor receptor (G-CSFR) is asymmetrically expressed in activated satellite cells. G-CSF positively affects the satellite cell population during multiple stages of differentiation in ex vivo cultured fibres. G-CSF could be important in developing an effective therapy for DMD based on its potential to modulate the supply of multiple stages of regenerated myocytes. This study shows that the G-CSF-G-CSFR axis is fundamentally important for long-term muscle regeneration, functional maintenance and lifespan extension in mouse models of DMD with varying severities.",

author = "Nozomi Hayashiji and Shinsuke Yuasa and Yuko Miyagoe-Suzuki and Mie Hara and Naoki Ito and Hisayuki Hashimoto and Dai Kusumoto and Tomohisa Seki and Shugo Tohyama and Masaki Kodaira and Akira Kunitomi and Shin Kashimura and Makoto Takei and Yuki Saito and Shinichiro Okata and Toru Egashira and Jin Endo and Toshikuni Sasaoka and Shin'ichi Takeda and Keiichi Fukuda",

note = "Funding Information: This study was supported in part by research grants from The Ministry of Education, Science and Culture, Japan; The Program for Promotion of Fundamental Studies in Health Science of the National Institute of Biomedical Innovation; The Ministry of Health Labour and Welfare; Health Labour Sciences Research Grant; Nakatomi Foundation; Japan Heart Foundation/Novartis Grant for Research Award on Molecular and Cellular Cardiology; SENSHIN Medical Research Foundation; Kimura Memorial Heart Foundation Research Grant; Japan Intractable Diseases Research Foundation, Japan; The Cell Science Research Foundation; The Tokyo Biochemical Research Foundation; Suzuken Memorial Foundation; and The Japan Foundation for Applied Enzymology. Publisher Copyright: {\textcopyright} 2015 Macmillan Publishers Limited. All rights reserved.",

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doi = "10.1038/ncomms7745",

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AU - Hayashiji, Nozomi

AU - Yuasa, Shinsuke

AU - Miyagoe-Suzuki, Yuko

AU - Hara, Mie

AU - Ito, Naoki

AU - Hashimoto, Hisayuki

AU - Kusumoto, Dai

AU - Seki, Tomohisa

AU - Tohyama, Shugo

AU - Kodaira, Masaki

AU - Kunitomi, Akira

AU - Kashimura, Shin

AU - Takei, Makoto

AU - Saito, Yuki

AU - Okata, Shinichiro

AU - Egashira, Toru

AU - Endo, Jin

AU - Sasaoka, Toshikuni

AU - Takeda, Shin'ichi

AU - Fukuda, Keiichi

N1 - Funding Information: This study was supported in part by research grants from The Ministry of Education, Science and Culture, Japan; The Program for Promotion of Fundamental Studies in Health Science of the National Institute of Biomedical Innovation; The Ministry of Health Labour and Welfare; Health Labour Sciences Research Grant; Nakatomi Foundation; Japan Heart Foundation/Novartis Grant for Research Award on Molecular and Cellular Cardiology; SENSHIN Medical Research Foundation; Kimura Memorial Heart Foundation Research Grant; Japan Intractable Diseases Research Foundation, Japan; The Cell Science Research Foundation; The Tokyo Biochemical Research Foundation; Suzuken Memorial Foundation; and The Japan Foundation for Applied Enzymology. Publisher Copyright: © 2015 Macmillan Publishers Limited. All rights reserved.

PY - 2015/4/13

Y1 - 2015/4/13

N2 - Duchenne muscular dystrophy (DMD) is a chronic and life-threatening disease that is initially supported by muscle regeneration but eventually shows satellite cell exhaustion and muscular dysfunction. The life-long maintenance of skeletal muscle homoeostasis requires the satellite stem cell pool to be preserved. Asymmetric cell division plays a pivotal role in the maintenance of the satellite cell pool. Here we show that granulocyte colony-stimulating factor receptor (G-CSFR) is asymmetrically expressed in activated satellite cells. G-CSF positively affects the satellite cell population during multiple stages of differentiation in ex vivo cultured fibres. G-CSF could be important in developing an effective therapy for DMD based on its potential to modulate the supply of multiple stages of regenerated myocytes. This study shows that the G-CSF-G-CSFR axis is fundamentally important for long-term muscle regeneration, functional maintenance and lifespan extension in mouse models of DMD with varying severities.

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G-CSF supports long-term muscle regeneration in mouse models of muscular dystrophy

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