Abstract
Genomic and non-genomic effects of estrogen and their crosstalk in the skeletal muscle are still poorly understood. We investigated the effects of estrogen on the proliferation of mouse myoblast cells and the properties of the membrane estrogen receptor (ER). The effect of estrogen on the proliferation did not change regardless of the culture medium and serum concentration. The ER protein in the post-nuclear fraction was dose-dependently increased after treatment with 17β-estradiol and BSA-17β-estradiol-conjugate, which was attenuated by high concentrations of tamoxifen and ICI 182-780. The amount of ER was also reduced by the presence of an ERK1/2 inhibitor, PD 98059 or a specific p38 inhibitor, SB 203580 in both presence and absence of estradiol. The newly-synthesized ER was increased by 17β-estradiol dose- and time-dependently. The time course of the increase of mRNA was almost paralleled by newly-synthesized ER. The newly-synthesized ER by estrogen was further increased by the protein kinase C (PKC) activator, TPA. These results suggest that ERs located at plasma membrane are the target of estrogen action in mouse skeletal myoblast cells. The estrogen-stimulated ER synthesis was induced via both genomic and non-genomic pathways involving the PKC/MAPK signaling system. [J Physiol Sci. 2008;58 Suppl:S69]
