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This version published online on May 4, 2006
Molecular Endocrinology, doi:10.1210/me.2005-0316
Molecular Endocrinology Vol. 0, No. 2006 200503161-
doi:10.1210/me.2005-0316
Copyright © 2006 by the Endocrine Society.
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Submitted on August 2, 2005
Accepted on April 25, 2006

Androgens, Progestins and Glucocorticoids Induce Follicle-Stimulating Hormone {beta}-Subunit Gene Expression at the Level of the Gonadotrope

Varykina G. Thackray, Shauna M. McGillivray, and Pamela L. Mellon*

Departments of Reproductive Medicine and Neurosciences, the Biomedical Sciences Graduate Program and the Center for Reproductive Science and Medicine, University of California, San Diego, La Jolla, CA 92093-0674

* To whom correspondence should be addressed. E-mail: pmellon{at}ucsd.edu.

Follicle-stimulating hormone (FSH) is produced by the pituitary gonadotrope to regulate gametogenesis. Steroid hormones, including androgens, progestins and glucocorticoids, have all been shown to stimulate expression of the FSH{beta} subunit in primary pituitary cells and rodent models. Understanding the molecular mechanisms of steroid induction of FSH{beta} has been difficult due to the heterogeneity of the anterior pituitary. Immortalized L{beta}T2 cells are a model of a mature gonadotrope cell and express the endogenous steroid receptor for each of the three hormones. Transient transfection of each receptor along with ligand treatment stimulates the mouse FSH{beta} promoter, but induction is severely diminished using receptors that lack the ability to bind DNA, indicating that induction is likely through direct DNA binding. All three steroid hormones act within the first 500 bp of the FSH{beta} promoter where six putative hormone response elements (HREs) exist. The -381 site is critical for FSH{beta} induction by all three steroid hormones, while the -197 and -139 sites contribute to maximal induction. Interestingly, the -273 and -230 sites are also necessary for androgen and progestin induction of FSH{beta}, but not for glucocorticoid induction. Additionally, we find that all three receptors bind the endogenous FSH{beta} promoter, in vivo, and specifically bind the -381 site in vitro, suggesting that the binding of the receptors to this element is critical for the induction of FSH{beta} by these 3-keto steroid hormones. Our data indicate that androgens, glucocorticoids and progestins act via their receptors to directly activate FSH{beta} gene expression in the pituitary gonadotrope.
Key words: androgen • progesterone • glucocorticoid • FSH • gonadotrope

NURSA Molecule Pages Link:

Nuclear Receptors:   ERα  |  ERβ  |  GR  |  PR  |  AR
Ligands:   Dexamethasone  |  17β-Estradiol  |  Dihydrotestosterone  |  Progesterone  |  R5020



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