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Galectin-3 and N-acetylglucosamine promote myogenesis and improve skeletal muscle function in the mdx model of Duchenne muscular dystrophy

Rancourt Ann, Dufresne Sébastien S., St-Pierre Guillaume, Levesque Julie-Christine, Nakamura Haruka, Kikuchi Yodai, Satoh Masahiko S., Frenette Jérôme et Sato Sachiko. (2018). Galectin-3 and N-acetylglucosamine promote myogenesis and improve skeletal muscle function in the mdx model of Duchenne muscular dystrophy. Faseb Journal, 32, (12), p. 6445-6455.

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URL officielle: https://doi.org/10.1096/fj.201701151RRR

Résumé

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), where mutations in the dystrophin gene disrupts the firm adhesion. In DMD patients, even moderate contraction causes damage, leading to progressive muscle degeneration. The damaged muscles are repaired through myogenesis. Consequently, myogenesis is highly active in DMD patients, 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 myogenesis. Galectin-3 is an oligosaccharide-binding protein and known to be involved in cell–cell interactions and cell–matrix interactions. Galectin-3 is expressed in myoblasts and skeletal muscle while its function in muscle remains elusive. In this study, we found evidence that galectin-3 and the monosaccharide N-acetylglucosamine, which increases the ligands (oligosaccharides) of galectin-3, promotes myogenesis in vitro. Moreover, in the mdx mouse model of DMD, treatment with N-acetylglucosamine increased the muscle force production. Our results demonstrate that treatment with N-acetylglucosamine can mitigate the burden of DMD.

Type de document:Article publié dans une revue avec comité d'évaluation
Volume:32
Numéro:12
Pages:p. 6445-6455
Version évaluée par les pairs:Non
Date:Décembre 2018
Sujets:Sciences naturelles et génie > Sciences naturelles > Biologie et autres sciences connexes
Sciences de la santé
Sciences de la santé > Sciences de l'activité physique et réadaptation
Sciences de la santé > Sciences médicales > Biochimie
Département, module, service et unité de recherche:Départements et modules > Département des sciences de la santé > Unité d'enseignement en physiothérapie
Mots-clés:Glycobiology, lectins, monosaccharides, muscular dystrophy, Duchenne, glycomics, glycomique, lectines, myopathie de Duchenne
Informations complémentaires:Version pré-publication
Déposé le:15 janv. 2019 02:59
Dernière modification:15 janv. 2019 02:59
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