Kinetics of store-operated Ca2+ influx evoked by endomembrane Ca2+-ATPase inhibitors in human platelets.

M.W.J. Vuist, M.A.H. Feijge, J.W.M. Heemskerk

Research output: Contribution to journalArticleAcademicpeer-review


Department of Human Biology, University of Maastricht, The Netherlands.

Influx of Ca2+ from the extracellular medium into the platelet cytosol is regulated by the Ca2+ content of intracellular Ca2+ stores. In this paper, we show that activation of this pathway of store-operated Ca2+ influx (SOCI) by the endomembrane Ca2+-ATPase inhibitors, thapsigargin and 2,5-di-(tert-butyl)-1,4-benzohydroquinone, is mediated by an intracellular factor that accumulates in time. We also describe that SOCI is stimulated by treatment of the platelets with low doses of primaquine, a compound known to inhibit intracellular vesicular transport at higher concentrations. The protein tyrosine kinase inhibitor, genistein, completely antagonized the stimulating and accelerating effects on SOCI of primaquine treatment. These results suggest that SOCI is controlled by a time-dependent factor, whose generation is stimulated by primaquine and protein tyrosine kinase activation.
Original languageEnglish
Pages (from-to)447-450
Number of pages4
JournalProstaglandins Leukotrienes and Essential Fatty Acids
Issue number4-5
Publication statusPublished - 1 Jan 1997

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