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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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February 1990,
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T Fujimoto, and
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