Regulation of steroidogenesis and cholesterol synthesis by prostaglandin F-2  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-2 alpha in vitro suppresses lipoprotein utilization. The objective of this study was to examine the mechanism by which PGF-2 alpha exerts this effect. Cultured bovine luteal cells received 0.25 microCi[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 less than 0.01), but caused a significant reduction in the amount of radioactivity in the cholesterol fraction. PGF-2 alpha treatment inhibited the increase in lipoprotein-induced progesterone synthesis (P less than 0.01), but did not prevent the reduction in de-novo cholesterol synthesis brought about by LDL or HDL. PGF-2 alpha alone reduced cholesterol synthesis (P less than 0.01), but it was not as effective as either LDL or HDL. Both lipoproteins and PGF-2 alpha also decreased the amount of radioactivity in the progesterone fraction (P less than 0.01), and the effect of PGF-2 alpha 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-2 alpha. Therefore, it is suggested that PGF-2 alpha allows entry of lipoprotein cholesterol into the cell, but prevents utilization for steroidogenesis. In addition, PGF-2 alpha alone can suppress cholesterol synthesis, as well as decrease conversion of cholesterol to progesterone.

Localization of prostaglandin F2 inhibition of lipoprotein use by bovine luteal cells

“…PGF2ll had no effect on 25-hydroxycholesterol-stimulated (Pate & Condon, 1989). These results would also support those of Rajkumar et al (1985Rajkumar et al ( , 1988 (Jordan, 1981;Pate & Condon, 1984;Kenny & Robinson, 1986;Benhaim et al, 1987;Alila et al, 1988;Pate & Nephew, 1988).…”

“…PGF2u has been shown to suppress luteinizing hormone (LH)-stimulated, 3',5'-cyclic adenosine monophosphate (cAMP)-stimulated (Jordan, 1981;Pate & Condon, 1984;Benhaim et al, 1987) and lipoprotein-stimulated (Pate & Nephew, 1988;Pate & Condon, 1989) progesterone produc¬ tion. However, PGF-,U has no effect on low-density lipoprotein (LDL) or high-density lipoprotein (HDL) uptake in bovine luteal cells (Pate & Condon, 1989), or on HDL binding (Rajkumar et al, 1985) or LDL binding (Rajkumar et al, 1988) in rat luteal cells, and thus PGF2a may allow uptake of lipoprotein-carried cholesterol into the cell but inhibit the subsequent use of cholesterol for steroidogenesis.…”

Expression and regulation of secreted phosphoprotein 1 in the bovine corpus luteum and effects on T lymphocyte chemotaxis

“…These treatment concentrations have been shown to affect bovine luteal cell function in vitro (Pate & Condon 1989, Benyo & Pate 1992, Townson & Pate 1996. After culture, media were removed and luteal cells were harvested to quantify SPP1 mRNA by quantitative PCR (qPCR) or to evaluate SPP1 protein expression via western blot.…”

Polar phospholipids from bovine endogenously oxidized low density lipoprotein interfere with follicular thecal function

“…The uptake of lipoprotein particle remnants and HDL is mediated via the scavenger receptor, class B, type I and LRP receptors (Acton et al 1996, Argov et al 2004. While intact LDL is known to stimulate luteal steroidogenesis (Pate & Condon 1989, Brannian et al 1995, oxidatively modified LDL (oxLDL) prepared in a laboratory setting has been reported to inhibit luteal progesterone production (Carroll et al 1992). Anti-steroidogenic and anti-gonadotrophic activities have been observed also for synthetic alkyl hydroperoxides (Kodaman et al 1994).…”