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 and Keiichi Fukuda
Additional contact information
Nozomi Hayashiji: Keio University School of Medicine, 35-Shinanomachi Shinjuku-ku, Tokyo 160-8582, Japan
Shinsuke Yuasa: Keio University School of Medicine, 35-Shinanomachi Shinjuku-ku, Tokyo 160-8582, Japan
Yuko Miyagoe-Suzuki: National Institute of Neuroscience, National Center of Neurology and Psychiatry
Mie Hara: Keio University School of Medicine, 35-Shinanomachi Shinjuku-ku, Tokyo 160-8582, Japan
Naoki Ito: National Institute of Neuroscience, National Center of Neurology and Psychiatry
Hisayuki Hashimoto: Keio University School of Medicine, 35-Shinanomachi Shinjuku-ku, Tokyo 160-8582, Japan
Dai Kusumoto: Keio University School of Medicine, 35-Shinanomachi Shinjuku-ku, Tokyo 160-8582, Japan
Tomohisa Seki: Keio University School of Medicine, 35-Shinanomachi Shinjuku-ku, Tokyo 160-8582, Japan
Shugo Tohyama: Keio University School of Medicine, 35-Shinanomachi Shinjuku-ku, Tokyo 160-8582, Japan
Masaki Kodaira: Keio University School of Medicine, 35-Shinanomachi Shinjuku-ku, Tokyo 160-8582, Japan
Akira Kunitomi: Keio University School of Medicine, 35-Shinanomachi Shinjuku-ku, Tokyo 160-8582, Japan
Shin Kashimura: Keio University School of Medicine, 35-Shinanomachi Shinjuku-ku, Tokyo 160-8582, Japan
Makoto Takei: Keio University School of Medicine, 35-Shinanomachi Shinjuku-ku, Tokyo 160-8582, Japan
Yuki Saito: Keio University School of Medicine, 35-Shinanomachi Shinjuku-ku, Tokyo 160-8582, Japan
Shinichiro Okata: Keio University School of Medicine, 35-Shinanomachi Shinjuku-ku, Tokyo 160-8582, Japan
Toru Egashira: Keio University School of Medicine, 35-Shinanomachi Shinjuku-ku, Tokyo 160-8582, Japan
Jin Endo: Keio University School of Medicine, 35-Shinanomachi Shinjuku-ku, Tokyo 160-8582, Japan
Toshikuni Sasaoka: Brain Research Institute, Niigata University
Shin’ichi Takeda: National Institute of Neuroscience, National Center of Neurology and Psychiatry
Keiichi Fukuda: Keio University School of Medicine, 35-Shinanomachi Shinjuku-ku, Tokyo 160-8582, Japan

Nature Communications, 2015, vol. 6, issue 1, 1-16

Abstract: 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.

Date: 2015
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DOI: 10.1038/ncomms7745

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