ESTRADIOL REGULATES GONADOTROPIN-RELEASING-HORMONE RECEPTOR NUMBER, GROWTH AND INOSITOL PHOSPHATE PRODUCTION IN ALPHA-T3-1 CELLS

被引:73
作者
MCARDLE, CA
SCHOMERUS, E
GRONER, I
POCH, A
机构
[1] Institute for Hormone and Fertility Research, University of Hamburg, Hamburg
关键词
GONADOTROPES; ALPHA-T3-1; CELL; GONADOTROPIN-RELEASING HORMONE; ESTRADIOL; PHOSPHOLIPASE-C; RECEPTOR;
D O I
10.1016/0303-7207(92)90237-Z
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Gonadal steroids act at the pituitary to regulate gonadotropin-releasing hormone (GnRH) receptor number and the responsiveness of gonadotropes to GnRH and can act at post-receptor sites to modulate Ca2+-mediated and protein kinase C-mediated signal-transducing pathways. However, such effects have been seen in the mixed cell population of primary cell cultures and may involve indirect effects on cells other than gonadotropes. Here, steroid effects on a recently described gonadotrope-derived cell line (alpha-T3-1 cells) have been assessed. In these cells estradiol, progesterone, testosterone and corticosterone all exerted trophic effects. Estradiol increased [H-3]thymidine incorporation with an EC50 of 10(-12) to 10(-11) M and this effect was blocked by keoxifene, an estrogen receptor antagonist. Estradiol also reduced binding of [I-125]buserelin (EC50 approximately 10(-11) M), an effect which appears to reflect a reduction in GnRH receptor number rather than a change in K(d). Estradiol also shifted the dose-response curve for GnRH-stimulated inositol phosphate (IP) accumulation rightward, increasing the EC50 for this GnRH effect by approximately 20-fold. Accordingly estradiol acts directly upon alpha-T3-1 cells not only to reduce GnRH receptor number, but also to reduce the efficiency of coupling of residual GnRH receptors to second messenger generation.
引用
收藏
页码:95 / 103
页数:9
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