ATP-triggered calcium signals in human neutrophils.

Abstract

There is evidence that ATP is an important extracellular factor regulating neutrophil functions. Indeed, extracellular ATP has been shown to stimulate neutrophil migration into sites of inflammation as well as adhesion of circulating cells to the endothelium1. This nucleotide also acts as a secretagogue for enhanced exocytosis of primary granules from neutrophils. Finally, it does improve the release of superoxide induced by fMLP, thereby acting as a priming agent for this response2. Extracellular ATP causes a transient increase in cytosolic level of Ca2+, which is known to be used as a second messenger to control many cellular processes including secretion, enzyme control, gene regulation, and apoptosis3. The Ca 2+ signal is a complex event that involves both intracellular Ca2+ pool release and extracellular Ca entry. Emptying of intracellular Ca2+ pools is the major trigger for activation of Ca entry during the generation of receptor-mediated Ca2+ signal. This capacitative mechanism, that has been termed store-operated Ca2+ entry, may be the basis by which the cells maintain elevated cytosolic free calcium concentration and replenish their intracellular Ca2+ stores in response to agonist stimulation. The importance of this signalling pathway has been recognised in numerous investigations and has received a great deal of attention.