Estrogens Potentiate the Stimulatory Effects of Follicle-Stimulating Hormone on N-Cadherin Messenger Ribonucleic Acid Levels in Cultured Mouse Sertoli Cells

Gonadal steroids and FSH are key regulators of Sertoli cell function. N-Cadherin (N-cad) is a calcium-dependent cell adhesion molecule that mediates Sertoli cell-germ cell interactions. We recently demonstrated that steroids, in particular estradiol, are potent regulators of testicular N-cad messeng...

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Bibliographic Details
Published in:Endocrinology (Philadelphia) 1997-01, Vol.138 (1), p.41-48
Main Authors: MacCalman, Colin D, Getsios, Spiro, Farookhi, Riaz, Blaschuk, Orest W
Format: Article
Language:English
Subjects:
17β-Estradiol
Calcium
Cell adhesion
Cell adhesion molecules
Cell interactions
Estrogens
Follicle-stimulating hormone
Hormones
mRNA
N-Cadherin
Sertoli cells
Sex hormones
Spermatogenesis
Steroids
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Summary:Gonadal steroids and FSH are key regulators of Sertoli cell function. N-Cadherin (N-cad) is a calcium-dependent cell adhesion molecule that mediates Sertoli cell-germ cell interactions. We recently demonstrated that steroids, in particular estradiol, are potent regulators of testicular N-cad messenger RNA (mRNA) levels in vivo. In view of the cooperative effects of steroids and FSH on Sertoli cell-germ cell interactions, we examined the combined effects of these hormones on N-cad mRNA levels in cultured mouse Sertoli cells. FSH was capable of increasing N-cad mRNA levels 2-fold in these cells. The effects of FSH on N-cad mRNA levels in cultured Sertoli cells were mimicked by cAMP-inducing agents. Treatment of the Sertoli cell cultures with FSH and estradiol stimulated N-cad mRNA levels 3-fold, whereas steroids alone had no effect on N-cad mRNA levels. These studies demonstrate that FSH and estradiol in combination are required to achieve maximal N-cad mRNA levels in cultured Sertoli cells. The results obtained from these studies substantiate the hypothesis that estrogens play a pivotal role in regulating spermatogenesis.
ISSN:0013-7227
1945-7170
DOI:10.1210/endo.138.1.4831