骨髓增生性疾病患者血小板钙离子运动异常。

T Fujimoto, K Fujimura, A Kuramoto
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引用次数: 0

摘要

我们研究了骨髓增生性疾病(MPD)患者血小板钙离子内流的异常。MPD血小板胞浆内45Ca2+内流低于正常对照组。为了确定低Ca2+内流是否是由膜糖蛋白(GP) IIb-IIIa复合物对Ca2+通道的功能异常引起的,我们研究了通过GP IIb-IIIa复合物重组为脂质体的Ca2+内流。将5例患者血小板中纯化的GP IIb-IIIa复合体重组为磷脂脂质体。通过囊内Fura-2荧光测量的Ca2+内流到脂质体中的2例患者较低。这些发现与这些血小板刺激后细胞内钙浓度的结果相一致。我们得出结论,GP IIb-IIIa的功能异常参与了MPD血小板中Ca2+内流受损的机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Abnormalities of calcium ion movement in platelets of patients with myeloproliferative disorders.

We investigated abnormalities in calcium ion influx in platelets of patients with myeloproliferative disorders (MPD). 45Ca2+ influx into the cytosol of MPD platelets was lower than that of normal controls. To determine whether the low Ca2+ influx is caused by a functional abnormality of membrane glycoprotein (GP) IIb-IIIa complex for Ca2+ channel or not, we investigated the Ca2+ influx through GP IIb-IIIa complex, which was reconstituted into liposomes. The purified GP IIb-IIIa complex from platelets of 5 patients was reconstituted into phospholipid liposomes. Ca2+ influx into the liposomes measured by fluorescence of intravesicular Fura-2 was lower in 2 of these patients. These findings corresponded with the results of intracellular calcium concentration after stimulation in these platelets. We concluded that functional abnormalities of GP IIb-IIIa is involved in the mechanism of impaired Ca2+ influx in MPD platelets.

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