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 journalArticle

25 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 languageEnglish
Article number6745
JournalNature Communications
Volume6
DOIs
Publication statusPublished - 2015 Apr 13

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Muscular Dystrophies
Granulocyte Colony-Stimulating Factor
muscles
regeneration
mice
Duchenne Muscular Dystrophy
Muscle
Regeneration
Granulocyte Colony-Stimulating Factor Receptors
Satellites
Muscles
Maintenance
maintenance
Asymmetric Cell Division
cells
Cells
cell division
exhaustion
homeostasis
muscle cells

ASJC Scopus subject areas

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

Cite this

G-CSF supports long-term muscle regeneration in mouse models of muscular dystrophy. / Hayashiji, Nozomi; Yuasa, Shinsuke; Miyagoe-Suzuki, Yuko; Hara, Mie; Ito, Naoki; Hashimoto, Hisayuki; Kusumoto, Dai; Seki, Tomohisa; Tohyama, Shugo; Kodaira, Masaki; Kunitomi, Akira; Kashimura, Shin; Takei, Makoto; Saito, Yuki; Okata, Shinichiro; Egashira, Toru; Endo, Jin; Sasaoka, Toshikuni; Takeda, Shin'ichi; Fukuda, Keiichi.

In: Nature Communications, Vol. 6, 6745, 13.04.2015.

Research output: Contribution to journalArticle

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
Hayashiji, Nozomi ; Yuasa, Shinsuke ; Miyagoe-Suzuki, Yuko ; Hara, Mie ; Ito, Naoki ; Hashimoto, Hisayuki ; Kusumoto, Dai ; Seki, Tomohisa ; Tohyama, Shugo ; Kodaira, Masaki ; Kunitomi, Akira ; Kashimura, Shin ; Takei, Makoto ; Saito, Yuki ; Okata, Shinichiro ; Egashira, Toru ; Endo, Jin ; Sasaoka, Toshikuni ; Takeda, Shin'ichi ; Fukuda, Keiichi. / G-CSF supports long-term muscle regeneration in mouse models of muscular dystrophy. In: Nature Communications. 2015 ; Vol. 6.
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