{"title":"Abnormalities of calcium ion movement in platelets of patients with myeloproliferative disorders.","authors":"T Fujimoto, K Fujimura, A Kuramoto","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 8","pages":"1542-8"},"PeriodicalIF":0.0000,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
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.