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Regulation of cytosolic free Ca2+ in cultured rat alveolar macrophages (NR8383)
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1997
Year
Lung InflammationImmunologyCell DeathCellular PharmacologyExperimental PharmacologyCellular PhysiologyOxidative StressInflammationMolecular PharmacologyAbstract Ca2+ MobilizationCell SignalingCell PhysiologyMolecular SignalingCa2+ InfluxMolecular PhysiologyReceptor (Biochemistry)Ion ChannelsMembrane BiologyExternal Ca2+PharmacologyCell BiologyPhagocyteSignal TransductionPhysiologyCytosolic Free Ca2+Cellular BiochemistryMedicine
Abstract Ca2+ mobilization in the rat alveolar macrophage cell line NR8383 was examined with the Ca2+-sensitive fluorescent probe Fura-2. ATP and norepinephrine elicited a 108 and 46% increase, respectively, in cytosolic free Ca2+ concentration ([Ca2+]i). Acetylcholine, nicotine, isoproterenol, substance P, and vasoactive intestinal polypeptide did not alter [Ca2+]i. Inositol 1,4,5-trisphosphate (IP3) formation was also activated by ATP. The carbohydraterich cell wall preparation, zymosan, induced a gradual [Ca2+]i increase only in the presence of external Ca2+, but did not activate IP3 formation. This increase was abolished by laminarin and by removal of extracellular Ca2+, suggesting that the [Ca2+]i increase was activated by β-glucan receptors and mediated by Ca2+ influx. This influx was significantly reduced by SKF96365, but not by nifedipine, ω-conotoxin GVIA, ω-agatoxin IVA, or flunarizine. These results suggest that release of intracellular Ca2+ in NR8383 cells is regulated by P2-purinoceptors and that zymosan causes Ca2+ influx via a receptor-operated pathway.