Prostaglandin F(2α) stimulates phosphatidylinositol 4,5-bisphosphate hydrolysis and mobilizes intracellular Ca2+ in bovine luteal cells

John S Davis, L. L. Weakland, D. A. Weiland

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Abstract

The present studies were conducted to determine whether prostaglandin F(2α) (PGF(2α)) stimulates the production of 'second messengers' derived from inositol phospholipid hydrolysis and increases intracellular free Ca2+ ([Ca2+](i)) in isolated bovine luteal cells. PGF(2α) provoked rapid (10 sec) and sustained (up to 60 min) increases in the levels of inositol mono-, bis-, and trisphosphates (InsP, InsP2, and InsP3, respectively). InsP3 was formed more rapidly than InsP2 or InsP after PGF(2α) treatment. In addition, PGF(2α) increased inositol phosphpholipid turnover, as evidenced by increased 32PO4 incorporation into phosphatidic acid and phosphatidyl-inositol. LiCl (1-20 mM) enhanced inositol phosphate accumulation in response to PGF(2α). Maximal increases in InsP3 occurred at 1 μM PGF(2α), with half-maximal stimulation occurring at 36 nM. The acute effects of PGF(2α) on InsP3 levels were independent of reductions in extracellular calcium. Prostaglandins E1 and E2 also stimulated increases in inositol phosphate levels, albeit to a lesser extent. PGF(2α) also induced rapid and concentration-dependent increases in [Ca2+](i) as measured by quin-2 fluorescence. The PGF(2α)-induced increases in [Ca2+](i) were maximal within 30 sec (approximately 2- to 3-fold), and [Ca2+](i) remained elevated for 8-10 min. The PGF(2α)-induced increases in [Ca2+](i) were also independent of extracellular calcium. These findings demonstrate that the action of PGF(2α) is coupled to the phospholipase C-InsP3 and diacylglycerol second messenger system in the corpus luteum.

Original languageEnglish (US)
Pages (from-to)3728-3732
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume84
Issue number11
DOIs
StatePublished - Jan 1 1987

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Luteal Cells
Prostaglandins F
Phosphatidylinositols
Hydrolysis
Inositol Phosphates
Second Messenger Systems
Inositol
Calcium
Phosphatidic Acids
Alprostadil
Corpus Luteum
Diglycerides
Type C Phospholipases
Dinoprostone
Fluorescence

ASJC Scopus subject areas

  • General

Cite this

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title = "Prostaglandin F(2α) stimulates phosphatidylinositol 4,5-bisphosphate hydrolysis and mobilizes intracellular Ca2+ in bovine luteal cells",
abstract = "The present studies were conducted to determine whether prostaglandin F(2α) (PGF(2α)) stimulates the production of 'second messengers' derived from inositol phospholipid hydrolysis and increases intracellular free Ca2+ ([Ca2+](i)) in isolated bovine luteal cells. PGF(2α) provoked rapid (10 sec) and sustained (up to 60 min) increases in the levels of inositol mono-, bis-, and trisphosphates (InsP, InsP2, and InsP3, respectively). InsP3 was formed more rapidly than InsP2 or InsP after PGF(2α) treatment. In addition, PGF(2α) increased inositol phosphpholipid turnover, as evidenced by increased 32PO4 incorporation into phosphatidic acid and phosphatidyl-inositol. LiCl (1-20 mM) enhanced inositol phosphate accumulation in response to PGF(2α). Maximal increases in InsP3 occurred at 1 μM PGF(2α), with half-maximal stimulation occurring at 36 nM. The acute effects of PGF(2α) on InsP3 levels were independent of reductions in extracellular calcium. Prostaglandins E1 and E2 also stimulated increases in inositol phosphate levels, albeit to a lesser extent. PGF(2α) also induced rapid and concentration-dependent increases in [Ca2+](i) as measured by quin-2 fluorescence. The PGF(2α)-induced increases in [Ca2+](i) were maximal within 30 sec (approximately 2- to 3-fold), and [Ca2+](i) remained elevated for 8-10 min. The PGF(2α)-induced increases in [Ca2+](i) were also independent of extracellular calcium. These findings demonstrate that the action of PGF(2α) is coupled to the phospholipase C-InsP3 and diacylglycerol second messenger system in the corpus luteum.",
author = "Davis, {John S} and Weakland, {L. L.} and Weiland, {D. A.}",
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T1 - Prostaglandin F(2α) stimulates phosphatidylinositol 4,5-bisphosphate hydrolysis and mobilizes intracellular Ca2+ in bovine luteal cells

AU - Davis, John S

AU - Weakland, L. L.

AU - Weiland, D. A.

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N2 - The present studies were conducted to determine whether prostaglandin F(2α) (PGF(2α)) stimulates the production of 'second messengers' derived from inositol phospholipid hydrolysis and increases intracellular free Ca2+ ([Ca2+](i)) in isolated bovine luteal cells. PGF(2α) provoked rapid (10 sec) and sustained (up to 60 min) increases in the levels of inositol mono-, bis-, and trisphosphates (InsP, InsP2, and InsP3, respectively). InsP3 was formed more rapidly than InsP2 or InsP after PGF(2α) treatment. In addition, PGF(2α) increased inositol phosphpholipid turnover, as evidenced by increased 32PO4 incorporation into phosphatidic acid and phosphatidyl-inositol. LiCl (1-20 mM) enhanced inositol phosphate accumulation in response to PGF(2α). Maximal increases in InsP3 occurred at 1 μM PGF(2α), with half-maximal stimulation occurring at 36 nM. The acute effects of PGF(2α) on InsP3 levels were independent of reductions in extracellular calcium. Prostaglandins E1 and E2 also stimulated increases in inositol phosphate levels, albeit to a lesser extent. PGF(2α) also induced rapid and concentration-dependent increases in [Ca2+](i) as measured by quin-2 fluorescence. The PGF(2α)-induced increases in [Ca2+](i) were maximal within 30 sec (approximately 2- to 3-fold), and [Ca2+](i) remained elevated for 8-10 min. The PGF(2α)-induced increases in [Ca2+](i) were also independent of extracellular calcium. These findings demonstrate that the action of PGF(2α) is coupled to the phospholipase C-InsP3 and diacylglycerol second messenger system in the corpus luteum.

AB - The present studies were conducted to determine whether prostaglandin F(2α) (PGF(2α)) stimulates the production of 'second messengers' derived from inositol phospholipid hydrolysis and increases intracellular free Ca2+ ([Ca2+](i)) in isolated bovine luteal cells. PGF(2α) provoked rapid (10 sec) and sustained (up to 60 min) increases in the levels of inositol mono-, bis-, and trisphosphates (InsP, InsP2, and InsP3, respectively). InsP3 was formed more rapidly than InsP2 or InsP after PGF(2α) treatment. In addition, PGF(2α) increased inositol phosphpholipid turnover, as evidenced by increased 32PO4 incorporation into phosphatidic acid and phosphatidyl-inositol. LiCl (1-20 mM) enhanced inositol phosphate accumulation in response to PGF(2α). Maximal increases in InsP3 occurred at 1 μM PGF(2α), with half-maximal stimulation occurring at 36 nM. The acute effects of PGF(2α) on InsP3 levels were independent of reductions in extracellular calcium. Prostaglandins E1 and E2 also stimulated increases in inositol phosphate levels, albeit to a lesser extent. PGF(2α) also induced rapid and concentration-dependent increases in [Ca2+](i) as measured by quin-2 fluorescence. The PGF(2α)-induced increases in [Ca2+](i) were maximal within 30 sec (approximately 2- to 3-fold), and [Ca2+](i) remained elevated for 8-10 min. The PGF(2α)-induced increases in [Ca2+](i) were also independent of extracellular calcium. These findings demonstrate that the action of PGF(2α) is coupled to the phospholipase C-InsP3 and diacylglycerol second messenger system in the corpus luteum.

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JO - Proceedings of the National Academy of Sciences of the United States of America

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