Cell-Surface Protein Profiling Identifies Distinctive Markers of Progenitor Cells in Human Skeletal Muscle

SummarySkeletal muscle contains two distinct stem/progenitor populations. One is the satellite cell, which acts as a muscle stem cell, and the other is the mesenchymal progenitor, which contributes to muscle pathogeneses such as fat infiltration and fibrosis. Detailed and accurate characterization of these progenitors in humans remains elusive. Here, we performed comprehensive cell-surface protein profiling of the two progenitor populations residing in human skeletal muscle and identified three previously unrecognized markers: CD82 and CD318 for satellite cells and CD201 for mesenchymal progenitors. These markers distinguish myogenic and mesenchymal progenitors, and enable efficient isolation of the two types of progenitors. Functional study revealed that CD82 ensures expansion and preservation of myogenic progenitors by suppressing excessive differentiation, and CD201 signaling favors adipogenesis of mesenchymal progenitors. Thus, cell-surface proteins identified here are not only useful markers but also functionally important molecules, and provide valuable insight into human muscle biology and diseases

Comparative analysis of G2 arrest after irradiation with 75 keV carbon-ion beams and 137Cs gamma-rays in a human lymphoblastoid cell line.

Heavy-ion beams are more effective than gamma-rays in causing G2 arrest. In this study, we investigated the expression of Wee1 and Cdc2 protein levels in order to analyze the G2 arrest caused by carbon-ion beam irradiation. Human lymphoblastoid TK6 cells were exposed to a 75 keV carbon-ion beam or 137Cs gamma-rays. Although the levels of Wee1 and Cdc2 protein were increased after exposure to either beam, Wee1 protein levels were influenced more by carbon-ion beam irradiation than by gamma-rays. To the contrary, Cdc2 protein levels were increased more by gamma-rays than by carbon-ion beams. These findings suggest that the G2 arrest produced by heavy-ion beams, such as the carbon-ion irradiation used in this study, might be associated with the overexpression of the Wee1 protein and of Cdc2 phosphorylation regulated by Wee1. Together, these events may act to prolong the length of G2 arrest