Sang Hyup Lee, Sang Yoon Kim, Yun Gu Gwon, Chanwoo Lee, Changhwan Kim, Ick Hyun Cho, Tae-Won Kim, Bong-Keun Choi
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Recombinant ADAMTS1 promotes muscle cell differentiation and alleviates muscle atrophy by repressing NOTCH1.
A disintegrin and metalloproteinase with thrombospondin motifs 1 (ADAMTS1) plays crucial roles in various biological processes, including myogenesis, by modulating the neurogenic locus notch homolog protein 1 (NOTCH1) signaling pathway. However, the mechanisms through which ADAMTS1 regulates myogenesis remain unclear. In this study, we generated recombinant ADAMTS1 mutants and determined their effects on muscle cell differentiation, focusing on the regulation of NOTCH1 signaling. Treatment of C2C12 cells with recombinant ADAMTS1 protein enhanced muscle cell differentiation. Meanwhile, ADAM10 treatment inhibited muscle differentiation through the activation of NOTCH1 cleavage. Recombinant ADAMTS1 reversed ADAM10-induced muscle cell atrophy by suppressing NOTCH1 activation and downregulating its target gene. Recombinant ADAMTS1 also alleviated dexamethasoneinduced muscle atrophy in a mouse model. In summary, our findings suggest that recombinant ADAMTS1 promotes muscle regeneration by suppressing NOTCH1 and highlight the potential of recombinant ADAMTS1 proteins in the treatment of muscle wasting disease. [BMB Reports 2024; 57(12): 539-545].
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The BMB Reports (BMB Rep, established in 1968) is published at the end of every month by Korean Society for Biochemistry and Molecular Biology. Copyright is reserved by the Society. The journal publishes short articles and mini reviews. We expect that the BMB Reports will deliver the new scientific findings and knowledge to our readers in fast and timely manner.
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