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Galectin‐3 and N ‐acetylglucosamine promote myogenesis and improve skeletal muscle function in the mdx model of Duchenne muscular dystrophy
Author(s) -
Rancourt Ann,
Dufresne Sébastien S.,
StPierre Guillaume,
Lévesque JulieChristine,
Nakamura Haruka,
Kikuchi Yodai,
Satoh Masahiko S.,
Frenette Jéôme,
Sato Sachiko
Publication year - 2018
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/fj.201701151rrr
Subject(s) - myogenesis , sarcolemma , duchenne muscular dystrophy , myocyte , skeletal muscle , basal lamina , itga7 , mdx mouse , microbiology and biotechnology , biology , muscular dystrophy , medicine , endocrinology , dystrophin , anatomy , genetics , ultrastructure
The muscle membrane, sarcolemma, must be firmly attached to the basal lamina. The failure of proper attachment results in muscle injury, which is the underlying cause of Duchenne muscular dystrophy (DMD), in which mutations in the dystrophin gene disrupts the firm adhesion. In patients with DMD, even moderate contraction causes damage, leading to progressive muscle degeneration. The damaged muscles are repaired through myogenesis. Consequently, myogenesis is highly active in patients with DMD, and the repeated activation of myogenesis leads to the exhaustion of the myogenic stem cells. Therefore, approaches to reducing the risk of the exhaustion are to develop a treatment that strengthens the interaction between the sarcolemma and the basal lamina and increases the efficiency of the myogenesis. Galectin‐3 is an oligosaccharide‐binding protein and is known to be involved in cell–cell interactions and cell–matrix interactions. Galectin‐3 is expressed in myoblasts and skeletal muscle, although its function in muscle remains elusive. In this study, we found evidence that galectin‐3 and the monosaccharide N ‐acetylglucosamine, which increases the synthesis of binding partners (oligosaccharides) of galectin‐3, promote myogenesis in vitro. Moreover, in the mdx mouse model of DMD, treatment with N ‐acetylglucosamine increased muscle‐force production. The results suggest that treatment with N ‐acetylglucosamine might mitigate the burden of DMD.—Rancourt, A., Dufresne, S. S., St‐Pierre, G., Levesque, J.‐C., Nakamura, H., Kikuchi, Y., Satoh, M. S., Frenette, J., Sato, S. Galectin‐3 and N ‐acetylglucosamine promote myogenesis and improve skeletal muscle function in the mdx model of Duchenne muscular dystrophy. FASEB J. 32, 6445–6455 (2018). www.fasebj.org