Thapsigargin inhibits Ca2+ entry into human neutrophil granulocytes.
The mechanism of Ca2+ entry after ligand binding to receptors on the surface of non-excitable cells is a current focus of interest. Considerable attention has been given to Ca2+ influx induced by emptying of intracellular pools. Thapsigargin, an inhibitor of microsomal Ca(2+)-ATPase, is an important tool in inducing store-regulated Ca2+ influx. In the present paper we show that, at concentrations above 500 nM, thapsigargin also has an opposite effect: it inhibits store-regulated Ca2+ influx into Fura-2-loaded human neutrophil granulocytes. As thapsigargin has been frequently applied at concentrations up to 2 microM, its inhibitory action on plasma-membrane Ca2+ fluxes deserves consideration.
Department of Physiology, Semmelweis Medical University, Budapest, Hungary.
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Geiszt
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Káldi
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Szeberényi
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Ligeti
D001692:Biological Transport; D002118:Calcium / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D006801:Humans; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism*; D010766:Phosphorylation; D013729:Terpenes / Q000494:pharmacology*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D019284:Thapsigargin
D013729:Terpenes; D019284:Thapsigargin; D013755:Tetradecanoylphorbol Acetate; D002118:Calcium