Testosterone Stimulates Follicle-Stimulating Hormone β Transcription via Activation of Extracellular Signal-Regulated Kinase: Evidence in Rat Pituitary Cells1
| Autor: | Kevin W. Aylor, Alan C. Dalkin, John C. Marshall, Daniel J. Haisenleder, Margaret A. Shupnik, Laura L. Burger, Heidi E. Walsh |
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| Rok vydání: | 2005 |
| Předmět: |
MAPK/ERK pathway
endocrine system medicine.medical_specialty Kinase Cell Biology General Medicine Gonadotropin-releasing hormone Biology Gonadotropic cell Follicle-stimulating hormone Endocrinology Reproductive Medicine Internal medicine Dihydrotestosterone medicine Signal transduction hormones hormone substitutes and hormone antagonists Endocrine gland medicine.drug |
| Zdroj: | Biology of Reproduction. 72:523-529 |
| ISSN: | 1529-7268 0006-3363 |
| DOI: | 10.1095/biolreprod.104.035196 |
| Popis: | 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 FSH beta transcriptional responses to T. These findings suggest that one site of T regulation of FSH beta transcription is through the selective stimulation of the ERK pathway. |
| Databáze: | OpenAIRE |
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