title: Stimulation of brook trout ovarian steroidogenesis by gonadotropins I and II is mediated by the cyclic adenosine 3',5'-monophosphate/protein kinase A pathway.
abstract: In teleosts, ovarian steroidogenesis is under the control of two gonadotropic hormones, GTH I and GTH II, that are structurally and functionally homologous to FSH and LH. The intracellular mechanisms by which GTH I and GTH II stimulate steroidogenesis in the teleost ovary are not well understood. The purpose of this study was to investigate the involvement of the cAMP/protein kinase A (PKA) and protein kinase C (PKC)/Ca2+ signaling pathways in the steroidogenic actions of GTH I and GTH II in the ovary of the brook trout (Salvelinus fontinalis). The cAMP/PKA pathway mediated the actions of GTH I before germinal vesicle breakdown (preGVBD) and GTH II after GVBD and before ovulation (preOV). Experimental increases in intracellular cAMP concentration mimicked the steroidogenic effects of GTH I and GTH II, and an antagonistic analog of cAMP partially blocked them. In addition, GTH I and GTH II stimulated the production of cAMP in preGVBD and preOV follicles, respectively. Activation of the PKC/Ca2+ pathway by a phorbol ester or a Ca2+ ionophore blocked the GTH I- and GTH II-induced steroid production, whereas inhibition of PKC by specific inhibitors potentiated the effects of GTH I. These results suggest that the cAMP/PKA signaling pathway mediates the stimulatory effects of GTH I and GTH II on steroidogenesis, and they also suggest the additional involvement of the PKC/Ca2+ signaling pathway in modulating the actions of gonadotropins in brook trout ovarian follicles.
authors.affiliation: School of Fisheries, University of Washington, Seattle 98195, USA. planas@porthos.bio.ub.es
authors.forename: J V
authors.initials: JV
authors.lastname: Planas
authors.forename: F W
authors.initials: FW
authors.lastname: Goetz
authors.forename: P
authors.initials: P
authors.lastname: Swanson
mesh_terms: D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D005576:Colforsin / Q000494:pharmacology; D000242:Cyclic AMP / Q000037:antagonists & inhibitors / Q000378:metabolism*; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004958:Estradiol / Q000096:biosynthesis; D005260:Female; D006065:Gonadotropins, Pituitary / Q000494:pharmacology*; D006908:Hydroxyprogesterones / Q000378:metabolism; D007476:Ionophores / Q000494:pharmacology; D009281:Naphthalenes / Q000494:pharmacology; D006080:Ovarian Follicle / Q000187:drug effects / Q000378:metabolism; D010053:Ovary / Q000187:drug effects* / Q000378:metabolism*; D011493:Protein Kinase C / Q000037:antagonists & inhibitors; D015398:Signal Transduction; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014337:Trout / Q000378:metabolism*
chemical_list: D004791:Enzyme Inhibitors; D006065:Gonadotropins, Pituitary; D006908:Hydroxyprogesterones; D007476:Ionophores; D009281:Naphthalenes; C007433:17,20-dihydroxy-4-pregnen-3-one; D005576:Colforsin; D000001:Calcimycin; D004958:Estradiol; D000242:Cyclic AMP; D017868:Cyclic AMP-Dependent Protein Kinases; D011493:Protein Kinase C; C058819:calphostin C; D013755:Tetradecanoylphorbol Acetate