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

Joy Lee Pate, W. A. Condon

Research output: Contribution to journalArticle

27 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)439-446
Number of pages8
JournalJournal of Reproduction and Fertility
Volume87
Issue number2
StatePublished - 1989

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Luteal Cells
Prostaglandins F
Lipoproteins
Cholesterol
Progesterone
HDL Lipoproteins
LDL Lipoproteins
Radioactivity
Sterols
Acetates
Steroids

All Science Journal Classification (ASJC) codes

  • Developmental Biology
  • Molecular Biology
  • Physiology
  • Embryology
  • Obstetrics and Gynecology

Cite this

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title = "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.",
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T1 - Regulation of steroidogenesis and cholesterol synthesis by prostaglandin F-2α and lipoproteins in bovine luteal cells

AU - Pate, Joy Lee

AU - Condon, W. A.

PY - 1989

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N2 - 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.

AB - 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.

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