Journal
NATURE COMMUNICATIONS
Volume 6, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms7745
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Funding
- Ministry of Education, Science and Culture, Japan
- Program for Promotion of Fundamental Studies in Health Science of the National Institute of Biomedical Innovation
- Ministry of Health Labour and Welfare
- Health Labour Sciences Research Grant
- Nakatomi Foundation
- Japan Heart Foundation/Novartis
- SENSHIN Medical Research Foundation
- Kimura Memorial Heart Foundation
- Japan Intractable Diseases Research Foundation, Japan
- Cell Science Research Foundation
- Tokyo Biochemical Research Foundation
- Suzuken Memorial Foundation
- Japan Foundation for Applied Enzymology
- Grants-in-Aid for Scientific Research [15J11847, 25282202, 26290029, 15K19018, 24590497, 26860583] Funding Source: KAKEN
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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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