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BOR - Papers in Press, published online ahead of print October 27, 2004.
Biol Reprod 2004, 10.1095/biolreprod.104.035196
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BIOLOGY OF REPRODUCTION 72, 523–529 (2005)
DOI: 10.1095/biolreprod.104.035196
© 2005 by the Society for the Study of Reproduction, Inc.

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

D.J. Haisenleder2, L.L. Burger, K.W. Aylor, A.C. Dalkin, H.E. Walsh, M.A. Shupnik, and J.C. Marshall

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 {alpha}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 {alpha}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






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Copyright © 2005 by the Society for the Study of Reproduction.