Fujimoto T, Fujimura K, Kuramoto A
Nihon Ketsueki Gakkai Zasshi. 1989 Dec;52(8):1542-8.
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.
我们研究了骨髓增殖性疾病(MPD)患者血小板中钙离子内流的异常情况。45Ca2+流入MPD血小板胞质溶胶的量低于正常对照组。为了确定低钙离子内流是否由膜糖蛋白(GP)IIb-IIIa复合物作为钙离子通道的功能异常所致,我们研究了通过重组到脂质体中的GP IIb-IIIa复合物的钙离子内流。从5例患者血小板中纯化的GP IIb-IIIa复合物被重组到磷脂脂质体中。通过囊泡内Fura-2荧光测量的钙离子流入脂质体的量在其中2例患者中较低。这些发现与这些血小板刺激后细胞内钙浓度的结果一致。我们得出结论,GP IIb-IIIa的功能异常参与了MPD血小板中钙离子内流受损的机制。