Progesterone production by hamster granulosa and luteal cells during short-term incubation. Effects of lipoproteins, compactin and 25-hydroxycholesterol.

Granulosa and luteal cells from immature, hormone-primed hamsters increased progesterone production in response to luteinizing hormone (LH) in a dose-dependent manner. Both cell types responded to 8-bromoadenosine 3':5'-cyclic monophosphate (8-Br-cAMP) with increased progesterone production. Lipoproteins (hamster or human) did not enhance progesterone production by either cell type in the presence of LH during short-term incubation; human high-density lipoprotein (HDL) inhibited progestin production. Compactin, an inhibitor of cholesterol biosynthesis, had no significant effect on progesterone production by either cell type. Granulosa and luteal cells increased progesterone production in response to 25-OH-cholesterol. The response to 25-OH-cholesterol was more rapid than that to LH. Increased progestin levels were apparent within 15 min of incubation whereas a response to LH was not seen until 30 min. LH in combination with 25-OH-cholesterol did not increase progesterone production above that seen with either agent alone. Cycloheximide blocked LH-stimulated steroidogenesis but not 25-OH-cholesterol-stimulated progestin production in both cell types. We conclude that 1) hamster granulosa and luteal cells rely upon endogenous, preformed cholesterol for the acute steroidogenic response to LH and 2) LH-stimulated steroidogenesis, but not 25-OH-cholesterol-stimulated steroidogenesis, is a cycloheximide-sensitive process which presumably involves an increase in the access of cellular cholesterol to the side-chain cleavage system.