TRPing out Platelet Calcium
TRPM7 (Transient Receptor Potential Melastatin-Like 7) Modulates Calcium Mobilization and Platelet Function via Phospholipase C Interactions
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Originally identified as coagulation factor IV, calcium (Ca2+) is now well established as a key cofactor in the formation of the tenase and prothrombinase complexes on the extracellular surfaces of activated platelets to ultimately mediate fibrin generation and hemostasis.1 Similarly, Ca2+ has long been known to serve an important intracellular role in orchestrating the cell biological responses of platelets in hemostatic plug formation.2–5 During the past several decades, as biochemical efforts have identified and refined roles for Ca2+ as an essential second messenger in virtually all cells,3 complementary studies of platelets have similarly detailed how spatiotemporal changes in intracellular Ca2+ levels regulate platelet granule secretion, cytoskeletal dynamics, aggregation, and other cell biological outputs underlying platelet physiology. On a general mechanistic level, changes in intracellular Ca2+ concentrations that trigger the cellular responses driving platelet function are solicited downstream of a variety of receptors that differentially activate phospholipase C (PLC) family members, resulting in inositol-1,4,5-trisphosphate (IP3) production and IP3R (IP3 receptor)-mediated release of Ca2+ from intracellular stores (Figure).4,6–9