Wegner J A, Martinez-Zaguilan R, Gillies R J, Hoyer P B
Department of Physiology, University of Arizona, Tucson 85724.
Endocrinology. 1991 Feb;128(2):929-36. doi: 10.1210/endo-128-2-929.
A previous study demonstrated that prostaglandin F2 alpha (PGF2 alpha) stimulates a transient increase in cytosolic free Ca2+ levels [( Ca2+]i) in ovine large luteal cells. In the present study, the magnitude of the PGF2 alpha (0.5 microM)-induced calcium transient in Hanks' medium (87 +/- 2 nM increase above resting levels) was reduced (P less than 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 PGF2 alpha-induced calcium transient. The inhibitory effect of PGF2 alpha 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 less than 0.05) in large cells incubated in Ca2(+)-free medium (27 +/- 4 nM; 70 +/- 6% control, respectively) or with 5 microM 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 less than 0.05) by conditions that increased (P less than 0.05) [Ca2+]i; that is LaCl3 ([Ca2+]i, 120 +/- 17 nM; progesterone, 82 +/- 8% control) and PGF2 alpha ([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 PGF2 alpha 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 PGF2 alpha-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.
先前的一项研究表明，前列腺素F2α（PGF2α）可刺激绵羊大黄体细胞胞质游离Ca2+水平[（Ca2+]i）短暂升高。在本研究中，在无Ca2+或无磷酸盐和碳酸盐的培养基中孵育的用fura-2负载的大黄体细胞中，PGF2α（0.5 microM）诱导的钙瞬变幅度（比静息水平升高87±2 nM）降低（P<0.05）但未完全消除（分别比静息水平高10±1 nM、32±6 nM）。用1 mM LaCl3（钙拮抗剂）预孵育2分钟可消除PGF2α诱导的钙瞬变。在无Ca2+培养基或加有LaCl3的培养基中，PGF2α对孕酮分泌的抑制作用降低。在无Ca2+培养基（分别为27±4 nM；70±6%对照）或用5 microM 5,5'-二甲基双-（O-氨基苯氧基）乙烷-N,N,N'N'-四乙酸（分别为40±2 nM；49±1%对照）孵育的大细胞中，静息[Ca2+]i水平和孕酮基础分泌均降低（P<0.05）。此外，增加（P<0.05）[Ca2+]i的条件可抑制（P<0.05）孕酮分泌；即LaCl3（[Ca2+]i，120±17 nM；孕酮，82±8%对照）和PGF2α（[Ca2+]i，102±10 nM；孕酮，82±3%对照）。在小黄体细胞中，在无Ca2+的Hanks液中孵育可降低静息[Ca2+]i水平和孕酮分泌（[Ca2+]i，28±2 nM；孕酮，71±6%对照），然而，LaCl3和PGF2α均未增加[Ca2+]i水平或抑制孕酮分泌。此处呈现的研究结果提供了证据，表明细胞外以及细胞内钙均有助于大细胞中PGF2α诱导的[Ca2+]i瞬变。此外，虽然大小细胞中都需要足够水平的[Ca2+]i来支持孕酮生成，但大细胞中最佳孕酮生成取决于适当的[Ca2+]i窗口。
