Prostaglandin F-induced calcium transient in ovine large luteal cells: II. Modulation of the transient and resting cytosolic free calcium alters progesterone secretion

J. A. Wegner, R. Martinez-Zaguilan, R. J. Gillies, Patricia B Hoyer

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Abstract

A previous study demonstrated that prostaglandin F (PGF) stimulates a transient increase in cytosolic free Ca2+ levels ([Ca2+]i) in ovine large luteal cells. In the present study, the magnitude of the PGF (0.5 μM)-induced calcium transient in Hanks' medium (87 ± 2 nM increase above resting levels) was reduced (P < 0.05) but not completely eliminated in fura-2 loaded large luteal cells incubated in Ca2+-free or phosphate- and carbonate-free medium (10 ± 1 nM, 32 ± 6 nM, above resting levels; respectively). Preincubation for 2 min with 1 mM LaCl3 (calcium antagonist) eliminated the PGF-induced calcium transient. The inhibitory effect of PGF on secretion of progesterone was reduced in Ca2+-free medium or medium plus LaCl3. Resting [Ca2+]i levels and basal secretion of progesterone were both reduced (P < 0.05) in large cells incubated in Ca2+-free medium (27 ± 4 nM; 70 ± 6% control, respectively) or with 5 μM 5,5′-dimethyl bis-(O-aminophenoxy)ethane-N,N,N′N′-tetraacetic acid (40 ± 2 nM; 49 ± 1% control; respectively). In addition, secretion of progesterone was inhibited (P < 0.05) by conditions that increased (P < 0.05) [Ca2+]i; that is LaCl3 ([Ca2+]i, 120 ± 17 nM; progesterone, 82 ± 8% control) and PGF ([Ca2+]i, 102 ± 10 nM; progesterone, 82 ± 3% control). In small luteal cells, resting [Ca2+]i levels and secretion of progesterone were reduced by incubation in Ca2+-free Hanks ([Ca2+]i, 28 ± 2 nM; progesterone, 71 ± 6% control), however, neither LaCl3 nor PGF increased [Ca2+]i levels or inhibited secretion of progesterone. The findings presented here provide evidence that extracellular as well as intracellular calcium contribute to the PGF-induced [Ca2+]i transient in large cells. Furthermore, whereas an adequate level of [Ca2+]i is required to support progesterone production in both small and large cells, optimal progesterone production in large cells depends upon an appropriate window of [Ca2+]i.

Original languageEnglish (US)
Pages (from-to)929-936
Number of pages8
JournalEndocrinology
Volume128
Issue number2
StatePublished - Feb 1991

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Luteal Cells
Dinoprost
Progesterone
Sheep
Calcium
Ethane
Fura-2
Carbonates
Phosphates

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Prostaglandin F-induced calcium transient in ovine large luteal cells : II. Modulation of the transient and resting cytosolic free calcium alters progesterone secretion. / Wegner, J. A.; Martinez-Zaguilan, R.; Gillies, R. J.; Hoyer, Patricia B.

In: Endocrinology, Vol. 128, No. 2, 02.1991, p. 929-936.

Research output: Contribution to journalArticle

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title = "Prostaglandin F2α-induced calcium transient in ovine large luteal cells: II. Modulation of the transient and resting cytosolic free calcium alters progesterone secretion",
abstract = "A previous study demonstrated that prostaglandin F2α (PGF2α) stimulates a transient increase in cytosolic free Ca2+ levels ([Ca2+]i) in ovine large luteal cells. In the present study, the magnitude of the PGF2α (0.5 μM)-induced calcium transient in Hanks' medium (87 ± 2 nM increase above resting levels) was reduced (P < 0.05) but not completely eliminated in fura-2 loaded large luteal cells incubated in Ca2+-free or phosphate- and carbonate-free medium (10 ± 1 nM, 32 ± 6 nM, above resting levels; respectively). Preincubation for 2 min with 1 mM LaCl3 (calcium antagonist) eliminated the PGF2α-induced calcium transient. The inhibitory effect of PGF2α on secretion of progesterone was reduced in Ca2+-free medium or medium plus LaCl3. Resting [Ca2+]i levels and basal secretion of progesterone were both reduced (P < 0.05) in large cells incubated in Ca2+-free medium (27 ± 4 nM; 70 ± 6{\%} control, respectively) or with 5 μM 5,5′-dimethyl bis-(O-aminophenoxy)ethane-N,N,N′N′-tetraacetic acid (40 ± 2 nM; 49 ± 1{\%} control; respectively). In addition, secretion of progesterone was inhibited (P < 0.05) by conditions that increased (P < 0.05) [Ca2+]i; that is LaCl3 ([Ca2+]i, 120 ± 17 nM; progesterone, 82 ± 8{\%} control) and PGF2α ([Ca2+]i, 102 ± 10 nM; progesterone, 82 ± 3{\%} control). In small luteal cells, resting [Ca2+]i levels and secretion of progesterone were reduced by incubation in Ca2+-free Hanks ([Ca2+]i, 28 ± 2 nM; progesterone, 71 ± 6{\%} control), however, neither LaCl3 nor PGF2α increased [Ca2+]i levels or inhibited secretion of progesterone. The findings presented here provide evidence that extracellular as well as intracellular calcium contribute to the PGF2α-induced [Ca2+]i transient in large cells. Furthermore, whereas an adequate level of [Ca2+]i is required to support progesterone production in both small and large cells, optimal progesterone production in large cells depends upon an appropriate window of [Ca2+]i.",
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T2 - II. Modulation of the transient and resting cytosolic free calcium alters progesterone secretion

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AU - Gillies, R. J.

AU - Hoyer, Patricia B

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N2 - A previous study demonstrated that prostaglandin F2α (PGF2α) stimulates a transient increase in cytosolic free Ca2+ levels ([Ca2+]i) in ovine large luteal cells. In the present study, the magnitude of the PGF2α (0.5 μM)-induced calcium transient in Hanks' medium (87 ± 2 nM increase above resting levels) was reduced (P < 0.05) but not completely eliminated in fura-2 loaded large luteal cells incubated in Ca2+-free or phosphate- and carbonate-free medium (10 ± 1 nM, 32 ± 6 nM, above resting levels; respectively). Preincubation for 2 min with 1 mM LaCl3 (calcium antagonist) eliminated the PGF2α-induced calcium transient. The inhibitory effect of PGF2α on secretion of progesterone was reduced in Ca2+-free medium or medium plus LaCl3. Resting [Ca2+]i levels and basal secretion of progesterone were both reduced (P < 0.05) in large cells incubated in Ca2+-free medium (27 ± 4 nM; 70 ± 6% control, respectively) or with 5 μM 5,5′-dimethyl bis-(O-aminophenoxy)ethane-N,N,N′N′-tetraacetic acid (40 ± 2 nM; 49 ± 1% control; respectively). In addition, secretion of progesterone was inhibited (P < 0.05) by conditions that increased (P < 0.05) [Ca2+]i; that is LaCl3 ([Ca2+]i, 120 ± 17 nM; progesterone, 82 ± 8% control) and PGF2α ([Ca2+]i, 102 ± 10 nM; progesterone, 82 ± 3% control). In small luteal cells, resting [Ca2+]i levels and secretion of progesterone were reduced by incubation in Ca2+-free Hanks ([Ca2+]i, 28 ± 2 nM; progesterone, 71 ± 6% control), however, neither LaCl3 nor PGF2α increased [Ca2+]i levels or inhibited secretion of progesterone. The findings presented here provide evidence that extracellular as well as intracellular calcium contribute to the PGF2α-induced [Ca2+]i transient in large cells. Furthermore, whereas an adequate level of [Ca2+]i is required to support progesterone production in both small and large cells, optimal progesterone production in large cells depends upon an appropriate window of [Ca2+]i.

AB - A previous study demonstrated that prostaglandin F2α (PGF2α) stimulates a transient increase in cytosolic free Ca2+ levels ([Ca2+]i) in ovine large luteal cells. In the present study, the magnitude of the PGF2α (0.5 μM)-induced calcium transient in Hanks' medium (87 ± 2 nM increase above resting levels) was reduced (P < 0.05) but not completely eliminated in fura-2 loaded large luteal cells incubated in Ca2+-free or phosphate- and carbonate-free medium (10 ± 1 nM, 32 ± 6 nM, above resting levels; respectively). Preincubation for 2 min with 1 mM LaCl3 (calcium antagonist) eliminated the PGF2α-induced calcium transient. The inhibitory effect of PGF2α on secretion of progesterone was reduced in Ca2+-free medium or medium plus LaCl3. Resting [Ca2+]i levels and basal secretion of progesterone were both reduced (P < 0.05) in large cells incubated in Ca2+-free medium (27 ± 4 nM; 70 ± 6% control, respectively) or with 5 μM 5,5′-dimethyl bis-(O-aminophenoxy)ethane-N,N,N′N′-tetraacetic acid (40 ± 2 nM; 49 ± 1% control; respectively). In addition, secretion of progesterone was inhibited (P < 0.05) by conditions that increased (P < 0.05) [Ca2+]i; that is LaCl3 ([Ca2+]i, 120 ± 17 nM; progesterone, 82 ± 8% control) and PGF2α ([Ca2+]i, 102 ± 10 nM; progesterone, 82 ± 3% control). In small luteal cells, resting [Ca2+]i levels and secretion of progesterone were reduced by incubation in Ca2+-free Hanks ([Ca2+]i, 28 ± 2 nM; progesterone, 71 ± 6% control), however, neither LaCl3 nor PGF2α increased [Ca2+]i levels or inhibited secretion of progesterone. The findings presented here provide evidence that extracellular as well as intracellular calcium contribute to the PGF2α-induced [Ca2+]i transient in large cells. Furthermore, whereas an adequate level of [Ca2+]i is required to support progesterone production in both small and large cells, optimal progesterone production in large cells depends upon an appropriate window of [Ca2+]i.

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