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Bridging molecules are secreted from the skeletal muscle and potentially regulate muscle differentiation

Muscle myogenesis is an essential step for muscle development and recovery. During muscle fusion, multiple molecules are thought to be necessary for the formation of normal myotubes. Milk fat globule-EGF factor 8 (MFG-E8) and Gas6 are phosphatidylserine-recognizing bridging molecules that are secret...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2020-01, Vol.522 (1), p.113-120
Main Authors: Chikazawa, Miho, Shimizu, Makoto, Yamauchi, Yoshio, Sato, Ryuichiro
Format: Article
Language:English
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Summary:Muscle myogenesis is an essential step for muscle development and recovery. During muscle fusion, multiple molecules are thought to be necessary for the formation of normal myotubes. Milk fat globule-EGF factor 8 (MFG-E8) and Gas6 are phosphatidylserine-recognizing bridging molecules that are secreted mainly from immune cells. In this study, we confirmed that these molecules are expressed and secreted from C2C12 cells. Mouse muscle and satellite cells also expressed these molecules. MFG-E8 was highly expressed and secreted in both undifferentiated and differentiated C2C12 cells. We observed that MFG-E8 and Gas6 were bound to the surface of differentiated C2C12 cells more compared with undifferentiated cells. Additionally, the treatment of recombinant MFG-E8 upregulated expression of myogenic genes and suppressed apoptosis during myogenesis in C2C12 cells. In this paper, we discuss the presence of novel functional molecules expressed and secreted in the skeletal muscle. The results of this study suggest that bridging molecules are one of the determinants of myogenesis or other muscle responses. •MFG-E8 and Gas6 are secretion factors from skeletal muscle.•Bridging molecule expression is regulated during muscle differentiation.•MFG-E8 and Gas6 specifically bind to the surface of differentiating myocytes.•MFG-E8 enhanced the differentiation of C2C12 cells.•MFG-E8 suppressed cell death during C2C12 differentiation.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2019.11.010