l-Anserine Increases Muscle Differentiation and Muscle Contractility in Human Skeletal Muscle Cells

l-Anserine, an imidazole peptide, has a varietyof physiologicalactivities, but its effects on skeletal muscle differentiation andmuscle contractile force remain unknown. Thus, in this study, we investigatedthe effect of l-anserine on muscle differentiation and musclecontractile force in human skeletal muscle cells. In two-dimensionalculture, 1 mu M l-anserine significantly increased themyotube diameters (26.5 +/- 1.71, 27.7 +/- 1.08, and 28.8 +/- 0.85 mu m with 0, 0.1, and 1 mu M l-anserine, respectively)and the expression levels of genes involved in muscle differentiationand the sarcomere structure. In three-dimensional culture, 1 mu M l-anserine significantly increased the contractile force ofengineered human skeletal muscle tissues cultured on a microdevice(1.99 +/- 0.30, 2.17 +/- 0.62, 2.66 +/- 0.39, and 3.28 +/- 0.85 mu N with 0, 0.1, 0.5, and 1 mu M l-anserine,respectively). l-Anserine also increased the myotube diametersand the proportion of myotubes with sarcomere structures in the culturedtissues. Furthermore, the histamine receptor 1 (H1R) antagonist attenuatedthe l-anserine-induced increase in the contractile force,suggesting the involvement of H1R in the mechanism of action of l-anserine. This study showed for the first time that l-anserine enhances muscle differentiation and muscle contractilityvia H1R.

Automated summary

In this study, the researchers investigated the effects of l-Anserine on muscle differentiation and muscle contractile force in human skeletal muscle cells. They found that l-Anserine significantly increased myotube diameters and the expression of genes involved in muscle differentiation and sarcomere structure. Additionally, l-Anserine also increased the contractile force of engineered human skeletal muscle tissues, and this effect was attenuated by a histamine receptor 1 (H1R) antagonist. These findings suggest that l-Anserine enhances muscle differentiation and contractility via H1R.