Differential role of protein kinase C in the action of luteinizing hormone-releasing hormone on hormone production in rat ovarian cells.
This study was undertaken to determine the involvement of arachidonic acid and protein kinase C in the actions of luteinizing hormone-releasing hormone on steroid and prostaglandin formation in the ovary. In primary culture of rat granulosa cells, treatment with 3 x 10(-7) mol/L melittin stimulates progesterone and prostaglandin E2 accumulation after a 5-hour culture period. Concomitant treatment of the cells with melittin and luteinizing hormone-releasing hormone or 12-0-tetradecanoylphorbol 13-acetate further enhances the stimulatory action of either luteinizing hormone-releasing hormone or 12-0-tetradecanoylphorbol 13-acetate by itself on prostaglandin E2 production. In contrast, no synergistic effects are observed on progesterone production by the same treatments. Treatment with luteinizing hormone-releasing hormone for 24 hours significantly decreases follicle-stimulating hormone-induced progesterone production by approximately 50%. Treatment of the cells with either follicle-stimulating hormone or luteinizing hormone-releasing hormone stimulates prostaglandin E2 production at least tenfold in the same cultures. When follicle-stimulating hormone and luteinizing hormone-releasing hormone are present concomitantly, they synergistically enhance prostaglandin E2 formation (p less than 0.01). Similar effects are observed with the phorbol ester, 12-0-tetradecanoylphorbol 13-acetate, which causes a dose-dependent inhibition of progesterone production by follicle-stimulating hormone whereas follicle-stimulating hormone-stimulated prostaglandin E2 formation is enhanced. Thus luteinizing hormone-releasing hormone-induced activation of protein kinase C may play multiple roles (stimulatory or inhibitory) in hormone production in the ovary.
Wang
J
J
Department of Obstetrics/Gynecology, University of British Columbia, Grace Hospital, Vancouver, Canada.
Lee
V
V
Leung
P C
PC
D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000494:pharmacology / Q000502:physiology; D015237:Dinoprost / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D005260:Female; D005640:Follicle Stimulating Hormone / Q000378:metabolism / Q000494:pharmacology; D007987:Gonadotropin-Releasing Hormone / Q000378:metabolism / Q000494:pharmacology*; D006107:Granulosa Cells / Q000378:metabolism; D008555:Melitten / Q000494:pharmacology; D010053:Ovary / Q000166:cytology* / Q000378:metabolism; D011374:Progesterone / Q000378:metabolism*; D011453:Prostaglandins / Q000378:metabolism*; D011458:Prostaglandins E / Q000096:biosynthesis; D011493:Protein Kinase C / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D013755:Tetradecanoylphorbol Acetate / Q000378:metabolism / Q000494:pharmacology; D013997:Time Factors
D001095:Arachidonic Acids; D011453:Prostaglandins; D011458:Prostaglandins E; D008555:Melitten; D016718:Arachidonic Acid; D007987:Gonadotropin-Releasing Hormone; D011374:Progesterone; D005640:Follicle Stimulating Hormone; D015237:Dinoprost; D011493:Protein Kinase C; D015232:Dinoprostone; D013755:Tetradecanoylphorbol Acetate