Abstract
In the present study primary cultures of rat granulosa cells obtained from diethylstilbestrol (DES)-primed immature rats were used to study the regulation of 17 β-hydroxysteroid dehydrogenase (17HSD) activity and type 1 expression via protein kinase A (PKA)- and C (PKC)-dependent pathways, and by several autocrine and/or paracrine growth factors. Follicle-stimulating hormone (FSH), 8-bromo-cyclic adenosine-3′,5′-monophosphate (8-Br-cAMP) and transforming growth factor β 1 (TGF β 1) strongly enhanced 17HSD activity and type 1 expression. The stimulatory effects of FSH and 8-Br-cAMP were further potentiated by TGF β 1. In contrast, neither phorbol-12-myristate-13-acetate (PMA), epidermal growth factor (EGF), transforming growth factor α (TGF α) nor fibroblast growth factor (bFGF) affected 17HSD activity or type 1 expression when given alone. However, they effectively neutralized the stimulatory effects of 8-Br-cAMP and FSH. The present data suggest that, in rat granulosa cells 17HSD type 1 expression is primarily induced by FSH acting via PKA-dependent pathway and the extent of the induction is modulated by PKC-dependent inhibition and autocrine/paracrine growth factors present in the ovary.
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