敲减DTX4表达抑制C2C12细胞成肌分化

DTX4（Deltex 4 homolog）蛋白属于Deltex家族成员|Deltex家族是Notch信号通路的调节因子. 已知Notch信号通路在成肌分化中发挥重要作用. 然而，DTX4是否参与调控肌肉发育尚未有报道. 本研究探索DTX4对成肌分化的影响及作用机制. 实时定量PCR和蛋白质印迹分析揭示，伴随小鼠C2C12成肌细胞（myoblast）分化为肌管（myotube）过程，成肌分化标志蛋白肌球蛋白重链（myosin heavy-chain，MyHC）、肌细胞生成素(myogenin)表达逐渐升高，DTX4 mRNA及蛋白质表达水平也逐渐升高. 通过顺序专一的siRNA敲减DTX4表达后，C2C12成肌细胞肌管面积和肌管融合指数明显减少|MyHC、肌细胞生成素蛋白表达水平明显降低|但ERK信号通路未见明显变化.上述结果表明，敲减DTX4表达抑制C2C12细胞成肌分化.我们的结果提示，DTX4可能参与C2C12细胞成肌分化.

Knock-down of DTX4 Inhibits C2C12 Myoblast Differentiation

Deltex 4 homolog（DTX4）belongs to the Deltex family and serves as a Notch signaling regulatory factor. Notch signaling plays an essential role in regulating myogenic differentiation. The present study explored the role of DTX4 in myogenic differentiation. RT qPCR and Western blot analysis showed that myogenic differentiation marker proteins of myosin heavy chain (MyHC) and myogenin were increased gradually during C2C12 cell differentiation from myoblasts to myotubes, where the DTX4 mRNA and protein levels were upregulated. Knocking down DTX4 in C2C12 by siRNA transfection decreased the protein levels of MyHC and myogenin, and consequently inhibited myotube formation and reduced the fusion index. No significant change in ERK signaling was observed. We concluded that DTX4 might be involved in the differentiation of murine C2C12 myoblasts into myotubes.