HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 72/3/523    most recent biolreprod.104.035196v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal My Folders Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Haisenleder, D.J. Articles by Marshall, J.C. Search for Related Content PubMed PubMed Citation Articles by Haisenleder, D.J. Articles by Marshall, J.C. Agricola Articles by Haisenleder, D.J. Articles by Marshall, J.C.

Testosterone Stimulates Follicle-Stimulating Hormone ß Transcription via Activation of Extracellular Signal-Regulated Kinase: Evidence in Rat Pituitary Cells¹

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

This study investigated whether estradiol (E₂) or testosterone (T) activate extracellular signal-regulated kinase (ERK) and calcium/calmodulin-dependent kinase II (Ca/CaMK II), as indicated by enzyme phosphorylation in rat pituitaries. In vivo studies used adult female rats given E₂, T, or empty silastic capsules (vehicle controls). Twenty-four hours later, the rats were given a single pulse of GnRH (300 ng) or BSA-saline (to controls) and killed 5 min later. GnRH stimulated a two- to three-fold rise in activated Ca/CaMK II, and E₂ and T had no effect on Ca/CaMK II activation. In contrast, both GnRH and T stimulated threefold increases in ERK activity, with additive effects seen following the combination of GnRH+T. E₂ had no effect on ERK activity. In T3 clonal gonadotrope cells, dihydrotestosterone did not activate ERK alone but enhanced and prolonged the ERK responses to GnRH, demonstrating direct effects on the gonadotrope. Thus, the ERK response to GnRH plus androgen was enhanced in both rat pituitary and T3 cells. In vitro studies with cultured rat pituitary cells examined the effect of GnRH±T in the presence of the mitogen-activated protein (MAP) kinase kinase inhibitor, PD-098059 (PD). Results showed that PD suppressed ERK activational and FSHß transcriptional responses to T. These findings suggest that one site of T regulation of FSHß transcription is through the selective stimulation of the ERK pathway.

¹ Supported by USPHS grants HD-33039 and HD-11489 to J.C.M. and NICHD/NIH through a cooperative agreement (U54-HD28934) as part of the Specialized Cooperative Centers Program in Reproductive Research (J.C.M., D.J.H., M.A.S.).

² Correspondence: D.J. Haisenleder, Aurbach Medical Research Building, P.O. Box 801412, University of Virginia Health Sciences Center, Charlottesville, VA 22908. FAX: 434 243 9143; djh2q{at}virginia.edu

This article has been cited by other articles:

				N. Pitteloud, A. A. Dwyer, S. DeCruz, H. Lee, P. A. Boepple, W. F. Crowley Jr., and F. J. Hayes The Relative Role of Gonadal Sex Steroids and Gonadotropin-Releasing Hormone Pulse Frequency in the Regulation of Follicle-Stimulating Hormone Secretion in Men J. Clin. Endocrinol. Metab., July 1, 2008; 93(7): 2686 - 2692. [Abstract] [Full Text] [PDF]

				T. Kowase, H. E. Walsh, D. S. Darling, and M. A. Shupnik Estrogen Enhances Gonadotropin-Releasing Hormone-Stimulated Transcription of the Luteinizing Hormone Subunit Promoters via Altered Expression of Stimulatory and Suppressive Transcription Factors Endocrinology, December 1, 2007; 148(12): 6083 - 6091. [Abstract] [Full Text] [PDF]

				H. A Ferris, H. E Walsh, J. Stevens, P. C Fallest, and M. A Shupnik Luteinizing Hormone Beta Promoter Stimulation by Adenylyl Cyclase and Cooperation with Gonadotropin-Releasing Hormone 1 in Transgenic Mice and LBetaT2 Cells Biol Reprod, December 1, 2007; 77(6): 1073 - 1080. [Abstract] [Full Text] [PDF]