Premium
Skeletal Muscle‐derived Cytokines Regulate Myogenesis by Modulating Cell Cycle Withdrawal
Author(s) -
Kim Dongwook,
Singh Nilmani,
Chen Jie
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.615.7
Subject(s) - myogenesis , myocyte , autocrine signalling , skeletal muscle , microbiology and biotechnology , paracrine signalling , biology , cell cycle , endocrinology , cell , receptor , genetics
Regenerative myogenesis after injury is a unique capacity of adult skeletal muscle to maintain normal tissue structure. This ability declines with aging or muscle diseases. Muscle regeneration consists of precisely organized processes such as cell cycle withdrawal followed by myocyte fusion. However, regulatory mechanisms of skeletal myogenesis remain incompletely understood. Interestingly, muscle cells express a variety of cytokines, which may play roles in skeletal myogenesis in an autocrine or paracrine manner. Previously, we performed an RNAi screen that revealed many cytokines as candidate regulators of myogenic differentiation. We have now identified several of those cytokines, including Tumor Necrosis Factor Superfamily Member 10 (Tnsfs10), Fas ligand (FasL) and C‐C Motif Chemokine Ligand 8 (Ccl8), as negative regulators of myogenesis. Strikingly, all those cytokines inhibit myogenic differentiation by preventing myoblasts from exiting the cell cycle. Together with our previous finding that Fms‐like tyrokine kinase 3 ligand (Flt3L) positively regulates myogenesis by promoting cell cycle exit of the myoblasts, our results have led us to propose that cell cycle withdrawal is a main checkpoint through which muscle‐expressed cytokines control myogenesis. Support or Funding Information NIH/NIAMS, R01AR048914