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Calcium signaling in platelets
Author(s) -
VARGASZABO D.,
BRAUN A.,
NIESWANDT B.
Publication year - 2009
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1111/j.1538-7836.2009.03455.x
Subject(s) - orai1 , trpc , microbiology and biotechnology , chemistry , phospholipase c , stim1 , cytosol , platelet activation , platelet , intracellular , calcium signaling , calcium , voltage dependent calcium channel , biophysics , receptor , transient receptor potential channel , biochemistry , biology , endoplasmic reticulum , immunology , organic chemistry , enzyme
Summary. Agonist‐induced elevation in cytosolic Ca 2+ concentrations is essential for platelet activation in hemostasis and thrombosis. It occurs through Ca 2+ release from intracellular stores and Ca 2+ entry through the plasma membrane (PM). Ca 2+ store release is a well‐established process involving phospholipase (PL)C‐mediated production of inositol‐1,4,5‐trisphosphate (IP 3 ), which in turn releases Ca 2+ from the intracellular stores through IP 3 receptor channels. In contrast, the mechanisms controlling Ca 2+ entry and the significance of this process for platelet activation have been elucidated only very recently. In platelets, as in other non‐excitable cells, the major way of Ca 2+ entry involves the agonist‐induced release of cytosolic sequestered Ca 2+ followed by Ca 2+ influx through the PM, a process referred to as store‐operated calcium entry (SOCE). It is now clear that stromal interaction molecule 1 (STIM1), a Ca 2+ sensor molecule in intracellular stores, and the four transmembrane channel protein Orai1 are the key players in platelet SOCE. The other major Ca 2+ entry mechanism is mediated by the direct receptor‐operated calcium (ROC) channel, P2X 1 . Besides these, canonical transient receptor potential channel (TRPC) 6 mediates Ca 2+ entry through the PM. This review summarizes the current knowledge of platelet Ca 2+ homeostasis with a focus on the newly identified Ca 2+ entry mechanisms.