Montarras D, Pinset C, Pérez M C, Ilan J, Gros F
Institut Pasteur, Département de Biologie moléculaire, Paris, France.
C R Acad Sci III. 1993 Sep;316(9):1025-31.
The contribution of autocrine production of insulin-like growth factor II (IGFII) to myogenic differentiation was studied in the mouse myogenic C2 cells. Permissive C2 cells were stably transfected with a vector generating antisense RNA complementary to IGF RNAs. Our results show that: (1) accumulation of IGFII mRNA is dramatically decreased (this mRNA is undetectable by RNA blotting); (2) accumulation of MyoD mRNA also becomes undetectable by RNA blot analysis; (3) the ability of the cells to differentiate, including the activation of myogenin and myosin genes, is severely compromised; (4) expression of the MyoD genes and the ability to differentiate are restored following the addition of insulin or IGF to the cells. Our observations indicate that the autonomous differentiation of myogenic cells requires autocrine production of IGF and raise the possibility that IGFII positively regulates expression of the MyoD gene, one of the members of the myogenic regulatory factor family.
在小鼠成肌C2细胞中研究了胰岛素样生长因子II(IGFII)自分泌产生对成肌分化的作用。用产生与IGF RNA互补的反义RNA的载体稳定转染许可性C2细胞。我们的结果表明:(1)IGFII mRNA的积累显著减少(通过RNA印迹法检测不到这种mRNA);(2)通过RNA印迹分析也检测不到MyoD mRNA的积累;(3)细胞的分化能力,包括肌细胞生成素和肌球蛋白基因的激活,受到严重损害;(4)在向细胞中添加胰岛素或IGF后,MyoD基因的表达和分化能力得以恢复。我们的观察结果表明,成肌细胞的自主分化需要IGF的自分泌产生,并增加了IGFII正向调节成肌调节因子家族成员之一MyoD基因表达的可能性。