American Journal of Physiology-Cell Physiology · 1989 · 27 citations · 14 references
Life SciencesCell BiologyImmunologyCell SignalingExocytosisSignal TransductionNeutrophil BiologyRespiratory PhysiologyNeutrophil Effector FunctionsNeutrophil Signaling PathwaysPhagocyte ActivationRespiratory Burst Effects
Activation of exocytosis and respiratory burst in rabbit neutrophils by the chemotactic peptide fMet-Leu-Phe is inhibited by Co2+. Inhibition is antagonized by extracellular Ca2+ and is dependent on the time of preincubation of cells with Co2+ before addition of activator. Co2+ inhibits the enhancement of 45Ca association that occurs during activation with fMet-Leu-Phe. Interference with Ca2+ translocation across the plasma membrane by Co2+ is probably not the cause of inhibition of neutrophil activation, because activation in the absence of extracellular Ca2+ is inhibited by Co2+. Activation of neutrophils by phorbol myristate acetate is inhibited at higher Co2+ concentrations than activation by fMet-Leu-Phe. Inhibition of the superoxide production by Co2+ occurs both in the presence or in the absence of cytochalasin B. Fluorescence of neutrophils loaded with quin2 is diminished by Co2+, indicating that Co2+ had entered into the cytoplasm. The results are compatible with the view that Co2+ inhibits exocytosis and respiratory burst in neutrophils by an interaction with a Ca2+-dependent intracellular target.
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A non-disruptive technique for loading calcium buffers and indicators into cells
Roger Y. Tsien · Nature · 1981 · 1.1K citations
Richard B. Johnston, Bernard B. Keele, H. P. Misra et al. · Journal of Clinical Investigation · 1975 · 706 citations · Full text