Insulin-like growth factor-I-induced androgen receptor activation is mediated by the PI3K/Akt pathway in C2C12 skeletal muscle cells |
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Authors: | Won Jun Lee |
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Affiliation: | (1) Department of Biochemical Sciences, University of Florence, Viale G.B. Morgagni 50, 50134 Florence, Italy;(2) Interuniversity Institute of Myology, Florence, Italy; |
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Abstract: | Although insulin-like growth factor-I (IGF-I) and androgen receptor (AR) are well known effectors of skeletal muscle, the
molecular mechanism by which signaling pathways integrating AR and IGF-I in skeletal muscle cells has not been previously
examined. In this study, the role of PI3K/Akt on IGF-I-induced gene expression and activation of AR in skeletal muscle cells
was investigated. C2C12 cells were treated with IGF-I in the absence or presence of inhibitors of PI3K/Akt pathway (LY294002
and Wortmannin). Inhibition of the PI3K/Akt pathway with LY294002 or Wortmannin led to a significant decrease in IGF-I-induced
AR phosphorylation and total AR protein expression. Furthermore, IGF-I-induced AR mRNA and skeletal α-actin mRNA were blocked
by LY294002 or Wortmannin. Confocal images showed that IGF-I-induced AR translocation from cytosol to nucleus was inhibited
significantly in response to treatment with LY294002 or Wortmannin. The present results suggest that modulating effect of
IGF-I on AR gene expression and activation in C2C12 mouse skeletal muscle cells is mediated at least in part by the PI3K/Akt
pathway. |
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