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离子钙对凝血酶诱导的人血小板GPIb/IX受体下调的影响。

Influence of ionized calcium on thrombin-induced down regulation of GPIb/IX receptors on human platelets.

作者信息

Rao G H, Peller J D, White J G

机构信息

Department of Laboratory Medicine, University of Minnesota Medical School, Minneapolis 55455, USA.

出版信息

Thromb Res. 1997 Jan 1;85(1):23-31. doi: 10.1016/s0049-3848(96)00218-6.

DOI:10.1016/s0049-3848(96)00218-6
PMID:8983122
Abstract

The influence of ionized calcium on the down-regulation of GPIb/IX receptors on human platelets was evaluated by flow cytometry using monoclonal antibodies. Addition of EDTA alone to a washed platelet suspension did not cause decreased monoclonal antibody binding to the cells. However, introduction of thrombin to the washed platelets containing EDTA resulted in a marked decrease in binding of monoclonal antibodies to the GPIb/IX receptors. If calcium at 1-3 mmol/L was added to buffered platelets instead of EDTA before thrombin, down-regulation was prevented or significantly reduced. Restoring calcium to EDTA platelets after the thrombin-stimulated down-regulation had been in progress for 1-3 minutes caused reversal of decreased antibody binding by GPIb/IX to near resting levels. Results demonstrate that extracellular calcium is a major factor regulating thrombin-induced down-regulation.

摘要

通过使用单克隆抗体的流式细胞术评估了离子钙对人血小板上糖蛋白Ib/IX(GPIb/IX)受体下调的影响。仅向洗涤后的血小板悬液中添加乙二胺四乙酸(EDTA)不会导致单克隆抗体与细胞的结合减少。然而,将凝血酶引入含有EDTA的洗涤血小板中会导致单克隆抗体与GPIb/IX受体的结合显著减少。如果在添加凝血酶之前,向缓冲的血小板中添加1-3毫摩尔/升的钙而非EDTA,则可防止或显著减少下调。在凝血酶刺激的下调过程进行1-3分钟后,向含有EDTA的血小板中恢复钙会使GPIb/IX抗体结合减少逆转至接近静息水平。结果表明,细胞外钙是调节凝血酶诱导的下调的主要因素。

相似文献

1
Influence of ionized calcium on thrombin-induced down regulation of GPIb/IX receptors on human platelets.离子钙对凝血酶诱导的人血小板GPIb/IX受体下调的影响。
Thromb Res. 1997 Jan 1;85(1):23-31. doi: 10.1016/s0049-3848(96)00218-6.
2
Down-regulation and redistribution of GPV/GPVf2, a subunit of von Willebrand factor receptor (GPIb/IX/V complex), on the surface membrane of thrombin-stimulated human platelets.凝血酶刺激的人血小板表面膜上血管性血友病因子受体(糖蛋白Ib/IX/V复合物)的一个亚基GPV/GPVf2的下调与重新分布。
Br J Haematol. 1999 Jan;104(1):55-63. doi: 10.1046/j.1365-2141.1999.01131.x.
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Influence of combined thrombin stimulation, surface activation, and receptor occupancy on organization of GPIb/IX receptors on human platelets.凝血酶联合刺激、表面活化及受体占据对人血小板上糖蛋白Ib/IX受体组装的影响
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Fate of the GPIb/IX receptor complex following activation of human platelets.人血小板激活后糖蛋白Ib/IX受体复合物的命运
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Downregulation of the platelet surface glycoprotein Ib-IX complex in whole blood stimulated by thrombin, adenosine diphosphate, or an in vivo wound.凝血酶、二磷酸腺苷或体内伤口刺激全血中血小板表面糖蛋白Ib-IX复合物的下调。
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Prelabeled glycoprotein Ib/IX receptors are not cleared from exposed surfaces of thrombin-activated platelets.预先标记的糖蛋白Ib/IX受体不会从凝血酶激活的血小板的暴露表面清除。
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Thrombin-induced GPIb-IX centralization on the platelet surface requires actin assembly and myosin II activation.凝血酶诱导的血小板表面糖蛋白Ib-IX集中需要肌动蛋白组装和肌球蛋白II激活。
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The activation-induced decrease in the platelet surface expression of the glycoprotein Ib-IX complex is reversible.激活诱导的糖蛋白Ib-IX复合物血小板表面表达降低是可逆的。
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Thrombin-induced inhibition of platelet agglutination by von Willebrand factor (vWF): reversal by ionized calcium.凝血酶诱导 von Willebrand 因子(vWF)抑制血小板聚集:离子钙逆转。
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Thrombin-induced changes in platelet membrane glycoproteins Ib, IX, and IIb-IIIa complex.凝血酶诱导的血小板膜糖蛋白Ib、IX和IIb-IIIa复合物的变化。
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