RT Journal Article
SR Electronic
T1 Galectin-3 and <em>N</em>-acetylglucosamine promote myogenesis and improve skeletal muscle function in the <em>mdx</em> model of Duchenne muscular dystrophy
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 203653
DO 10.1101/203653
A1 Rancourt, Ann
A1 Dufresne, Sébastien
A1 St-Pierre, Guillaume
A1 Lévesque, Julie-Christine
A1 Nakamura, Haruka
A1 Kikuchi, Yodai
A1 Satoh, Masahiko S.
A1 Frenette, Jérôme
A1 Sato, Sachiko
YR 2017
UL http://biorxiv.org/content/early/2017/10/16/203653.abstract
AB 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.