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血小板中游离钙的细胞质浓度受环磷酸腺苷生成刺激剂(前列腺素D2、前列腺素E1、福斯高林)的控制。

The cytoplasmic concentration of free calcium in platelets is controlled by stimulators of cyclic AMP production (PGD2, PGE1, forskolin).

作者信息

Feinstein M B, Egan J J, Sha'afi R I, White J

出版信息

Biochem Biophys Res Commun. 1983 Jun 15;113(2):598-604. doi: 10.1016/0006-291x(83)91768-0.

DOI:10.1016/0006-291x(83)91768-0
PMID:6307295
Abstract

Maximal stimulation of platelets with thrombin results in a rapid increase in cytoplasmic Ca2+ (from 0.1 microM to 1-3 microM), as measured with the fluorescent intracellular Ca2+ indicator Quin-2. Prior addition of the adenylate cyclase stimulators PGD2, PGE1 or forskolin inhibited the rise in cytoplasmic Ca2+. When added after the maximal response to thrombin was attained adenylate cyclase stimulators caused a rapid fall of cytoplasmic Ca2+ back to the original "resting" level. This effect coincides with the reversal of thrombin-induced, Ca2+-dependent protein phosphorylation, and cytoskeleton assembly. It is suggested that cAMP-dependent reactions maintain low levels of cytoplasmic Ca2+ by promoting transport and/or binding of Ca2+.

摘要

用凝血酶对血小板进行最大刺激会导致细胞质Ca2+迅速增加(从0.1微摩尔升至1 - 3微摩尔),这是用荧光细胞内Ca2+指示剂喹啉-2测量得出的结果。预先添加腺苷酸环化酶刺激剂前列腺素D2、前列腺素E1或福斯高林可抑制细胞质Ca2+的升高。当在达到对凝血酶的最大反应后添加时,腺苷酸环化酶刺激剂会使细胞质Ca2+迅速降至原来的“静息”水平。这种效应与凝血酶诱导的、Ca2+依赖性蛋白磷酸化及细胞骨架组装的逆转相吻合。有人提出,cAMP依赖性反应通过促进Ca2+的转运和/或结合来维持细胞质Ca2+的低水平。

相似文献

1
The cytoplasmic concentration of free calcium in platelets is controlled by stimulators of cyclic AMP production (PGD2, PGE1, forskolin).血小板中游离钙的细胞质浓度受环磷酸腺苷生成刺激剂(前列腺素D2、前列腺素E1、福斯高林)的控制。
Biochem Biophys Res Commun. 1983 Jun 15;113(2):598-604. doi: 10.1016/0006-291x(83)91768-0.
2
Cytoplasmic Ca2+ in platelets is controlled by cyclic AMP: antagonism between stimulators and inhibitors of adenylate cyclase.血小板中的细胞质钙离子受环磷酸腺苷(cAMP)调控:腺苷酸环化酶刺激剂与抑制剂之间的拮抗作用。
Biochem Biophys Res Commun. 1984 Apr 30;120(2):579-85. doi: 10.1016/0006-291x(84)91294-4.
3
Reversal of thrombin-induced myosin phosphorylation and the assembly of cytoskeletal structures in platelets by the adenylate cyclase stimulants prostaglandin D2 and forskolin.
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4
Receptor (norepinephrine), P-site (2',5'-dideoxyadenosine), and calcium-mediated inhibition of prostaglandin and forskolin-activated cyclic AMP-generating systems in human platelets.人血小板中受体(去甲肾上腺素)、P 位点(2',5'-二脱氧腺苷)以及钙介导的对前列腺素和福斯高林激活的环磷酸腺苷生成系统的抑制作用
J Cyclic Nucleotide Protein Phosphor Res. 1985;10(3):229-45.
5
Cytochemical localization of adenylate cyclase in the dense tubule system of human blood platelets stimulated by forskolin, prostacyclin and prostaglandin D2.福斯高林、前列环素和前列腺素D2刺激下人血小板致密小管系统中腺苷酸环化酶的细胞化学定位
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6
Effects of activation of protein kinase C on the agonist-induced stimulation and inhibition of cyclic AMP formation in intact human platelets.蛋白激酶C激活对完整人血小板中激动剂诱导的环磷酸腺苷生成的刺激和抑制作用。
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Novel mechanism of heterologous desensitization of adenylate cyclase: prostaglandins bind with different affinities to both stimulatory and inhibitory receptors on platelets.腺苷酸环化酶异源脱敏的新机制:前列腺素以不同亲和力与血小板上的刺激性和抑制性受体结合。
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Effect of cyclic AMP on cytoplasmic free calcium in human platelets stimulated by thrombin: direct measurement with quin2.环磷酸腺苷对凝血酶刺激的人血小板胞质游离钙的影响:用喹啉-2进行直接测量
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Refractoriness of diabetic platelets to inhibitory prostaglandins.
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10
Effects of prostaglandin I2 and forskolin on the secretion from platelets evoked at basal concentrations of cytoplasmic free calcium by thrombin, collagen, phorbol ester and exogenous diacylglycerol.前列腺素I2和福斯高林对凝血酶、胶原蛋白、佛波酯和外源性二酰基甘油在细胞质游离钙基础浓度下诱发的血小板分泌的影响。
Biochem J. 1984 Sep 15;222(3):833-6. doi: 10.1042/bj2220833.

引用本文的文献

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Laropiprant attenuates EP3 and TP prostanoid receptor-mediated thrombus formation.拉罗匹坦可减轻 EP3 和 TP 前列腺素受体介导的血栓形成。
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Inhibition of inositol 1,4,5-trisphosphate-induced Ca2+ release by cAMP-dependent protein kinase in a living cell.环磷酸腺苷依赖性蛋白激酶对活细胞中肌醇1,4,5-三磷酸诱导的钙离子释放的抑制作用
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6
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Proc Natl Acad Sci U S A. 1984 May;81(10):3113-7. doi: 10.1073/pnas.81.10.3113.
7
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