Fam210a is a novel protein regulating muscle mass and strength in mice in vivo. However, detailed effects of Fam210a on the function of myoblasts as well as modulators of Fam210a are still unknown. We, thus, investigated (1) the roles of Fam210a in myoblast differentiation, proliferation, apoptosis and degradation, and (2) the factors that regulate Fam210a expression in murine C2C12 cells. We found that the level of Fam210a mRNA was reduced during myoblast differentiation. Reduction in endogenous Fam210a levels by siRNA suppressed mRNA levels of myogenic factors (Pax7, Myf5, Myogenin, and Mhc) and a muscle degradation factor (Murf1). On the other hand, Fam210a siRNA did not affect mRNA encoding the apoptotic factors Bcl-2 and Bax and the extent of apoptosis as measured by ELISA in C2C12 cells. In contrast, Fam210a siRNA increased the mRNA level of Mmp-12, which induces osteoclastogenesis. Interestingly, insulin and 1,25(OH)2D, which are known to affect cell metabolism and muscle function, significantly increased the level of Fam210a mRNA in a dose-dependent manner. In addition, a PI3-kinase inhibitor and reduction in endogenous levels of the vitamin D receptor (VDR) by siRNA suppressed insulin- and 1,25(OH)2D-induced expression of Fam210a, respectively. In conclusion, Fam210a might enhance myoblast differentiation and proteolysis. Moreover, insulin and 1,25(OH)2D may induce myoblast differentiation and degradation by enhancing the expression of Fam210a.

中文翻译：

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Fam210a的调节剂和Fam210a在成肌细胞功能中的作用。

Fam210a是一种新型蛋白，可在体内调节小鼠的肌肉质量和强度。但是，Fam210a对成肌细胞功能以及Fam210a调节剂的详细作用仍是未知的。因此，我们研究了（1）Fam210a在成肌细胞分化，增殖，凋亡和降解中的作用，以及（2）调节Fam210a在鼠C2C12细胞中表达的因子。我们发现成肌细胞分化过程中Fam210a mRNA的水平降低。siRNA降低内源性Fam210a水平抑制了肌源性因子（Pax7，Myf5，Myogenin和Mhc）和肌肉降解因子（Murf1）的mRNA水平。另一方面，如通过ELISA在C2C12细胞中测量的，Fam210a siRNA不影响编码凋亡因子Bcl-2和Bax的mRNA以及细胞凋亡的程度。相反，Fam210a siRNA增加Mmp-12的mRNA水平，从而诱导破骨细胞生成。有趣的是，已知会影响细胞代谢和肌肉功能的胰岛素和1,25（OH）2D以剂量依赖的方式显着增加Fam210a mRNA的水平。此外，PI3激酶抑制剂和siRNA降低维生素D受体（VDR）的内源性水平分别抑制了胰岛素和1,25（OH）2D诱导的Fam210a表达。总之，Fam210a可能增强成肌细胞的分化和蛋白水解作用。此外，胰岛素和1,25（OH）2D可能通过增强Fam210a的表达来诱导成肌细胞分化和降解。以剂量依赖性方式显着增加Fam210a mRNA的水平。此外，PI3激酶抑制剂和siRNA降低维生素D受体（VDR）的内源性水平分别抑制了胰岛素和1,25（OH）2D诱导的Fam210a表达。总之，Fam210a可能增强成肌细胞的分化和蛋白水解。此外，胰岛素和1,25（OH）2D可能通过增强Fam210a的表达来诱导成肌细胞分化和降解。以剂量依赖性方式显着增加Fam210a mRNA的水平。此外，PI3激酶抑制剂和siRNA降低维生素D受体（VDR）的内源性水平分别抑制了胰岛素和1,25（OH）2D诱导的Fam210a表达。总之，Fam210a可能增强成肌细胞的分化和蛋白水解作用。此外，胰岛素和1,25（OH）2D可能通过增强Fam210a的表达来诱导成肌细胞分化和降解。