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Regulation of Luteinizing Hormone-ß and Follicle-Stimulating Hormone (FSH)-ß Gene Transcription by Androgens: Testosterone Directly Stimulates FSH-ß Transcription Independent from Its Role on Follistatin Gene Expression

Division of Endocrinology, Department of Internal Medicine, and the Center for Research in Reproduction, University of Virginia, Charlottesville, Virginia 22908

Address all correspondence and requests for reprints to: Laura L. Burger, University of Virginia, Department of Internal Medicine, P.O. Box 801412, Charlottesville, Virginia 22908. E-mail: lburger{at}virginia.edu.

The gonadotropin ß-subunit mRNAs are differentially regulated by androgens. Testosterone (T) suppresses LH-ß and increases FSH-ß. We aimed to determine whether androgens regulate LH-ß and FSH-ß transcription [as measured by changes in primary transcript (PT)] and to determine whether androgens act directly on FSH-ß or via the intrapituitary activin/follistatin (FS) system. In castrate + GnRH antagonist-treated rats, T increased FSH-ß PT between 3 and 48 h. In contrast, T suppressed LH-ß PT. The increases in FSH-ß mRNA and PT were associated with reduced FS mRNA. Activin ßB mRNA was modestly suppressed. The increase in FSH-ß PT after T was androgen specific. Both T and dihydrotestosterone (DHT) increased FSH-ß PT 2-fold and decreased both FS and ßB mRNA. Estradiol suppressed FSH-ß PT 3-fold and had no effect on FS or ßB mRNAs. LH-ß PT was suppressed by DHT. To determine whether T stimulation of FSH-ß PT reflected a decrease in pituitary FS, we gave androgen in the presence of exogenous FS in vitro. T and DHT increased FSH-ß PT 2- to 3-fold. FS alone decreased FSH-ß PT 40% but did not diminish the increase FSH-ß PT in response to T. T, DHT, and FS did not affect FS mRNA, ßB mRNA, or LH-ß PT. In conclusion, androgens acting directly on the pituitary increase FSH-ß and decrease LH-ß transcription. The increase in FSH-ß PT in response to T was androgen specific and occurs in the presence of excess FS, suggesting that T stimulates FSH-ß transcription independently of modulation of FS.

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