Regulation of steroidogenesis and cholesterol synthesis by prostaglandin F-2α and lipoproteins in bovine luteal cells

Abstract

Bovine luteal cells can utilize low density lipoprotein (LDL) or high density lipoprotein (HDL) as a source of cholesterol for steroidogenesis, and administration of PGF-2α in vitro suppresses lipoprotein utilization. The objective of this study was to examine the mechanism by which PGF-2α exerts this effect. Cultured bovine luteal cells received 0.25 μCi[14C]acetate/ml, to assess rates of de-novo sterol and steroid synthesis, with or without lipoproteins. Both LDL and HDL enhanced progesterone production (P < 0.01), but caused a significant reduction in the amount of radioactivity in the cholesterol fraction. PGF-2α treatment inhibited the increase in lipoprotein-induced progesterone synthesis (P < 0.01), but did not prevent the reduction in de-novo cholesterol synthesis brought about by LDL and HDL. PGF-2α alone reduced cholesterol synthesis (P < 0.01), but it was not as effective as either LDL or HDL. Both lipoproteins and PGF-2α also decreased the amount of radioactivity in the progesterone fraction (P < 0.01), and the effect of PGF-2α was similar to that of the lipoproteins. It is concluded that lipoproteins can enhance progesterone production and also suppress de-novo cholesterol synthesis in bovine luteal cells, but only the former effect of lipoproteins is inhibited by PGF-2α. Therefore, it is suggested that PGF-2α allows entry of lipoprotein cholesterol into the cell, but prevents utilization for steroidogenesis. In addition, PGF-2α alone can suppress cholesterol synthesis, as well as decrease conversion of cholesterol to progesterone.