Acidic Ca(2+) stores in platelets

Changes in cytosolic free Ca²⁺ concentration play a pivotal role in the regulation of platelet functions, from secretion of autocrine and procoagulant factors to reversible or irreversible aggregation. It has long been recognized that platelet agonists release Ca²⁺ accumulated into the dense tubular system, the analogue of the endoplasmic reticulum. However, current evidence indicates that Ca²⁺ can also be stored and released from a number of acidic organelles, including lysosomes and lysosome-related organelles. Ca²⁺ release from the dense tubular system is mediated through phospholipase C-dependent synthesis of inositol 1,4,5-trisphosphate, whereas Ca²⁺ efflux from the acidic stores seems to be associated to the second messenger nicotinic acid adenine dinucleotide phosphate. The biochemical and biophysical properties of both Ca²⁺ stores in platelets have been reported to show significant differences. Selective discharge of one or both stores depends on the platelet agonist and the concentration used, which further supports the complexity of the Ca²⁺ signals that regulate platelet function. In this paper, we summarize the current knowledge on the role of acidic organelles in agonist-evoked Ca²⁺ mobilization and highlight recent progress in understanding the functional aspects of the acidic Ca²⁺ stores in Ca²⁺ signalling and platelet physiology.