A rise in cytosolic calcium concentration ([Ca2+]cyt) is central to platelet activation. Agonists stimulate a rise in [Ca2+]cyt through a combination of Ca2+ release from intracellular stores located in the dense tubular system (DTS) and acidic organelles as well as Ca2+ entry across the plasma membrane via several channel types. [Ca2+]cyt may be reduced by Ca2+ sequestration into the intracellular stores by sarco-endoplasmic reticulum Ca2+-ATPases (SERCAs) and via a H+-dependent mechanism, whilst Ca2+ may be removed across the plasma membrane by plasma membrane Ca2+-ATPases (PMCAs) and by Na+/Ca2+ exchangers (NCXs). Ca2+ signals are shaped by differential employment of these basic Ca2+ entry and removal processes and by Ca2+ buffers present in the platelet cytosol and other cellular compartments. In turn, Ca2+ signals can be transduced into a number of platelet responses by an array of effector proteins which may be activated in some cases by Ca2+ signals confined to specific cellular microdomains.
CITATION STYLE
Harper, A. G. S., & Sage, S. O. (2017). Platelet signalling: Calcium. In Platelets in Thrombotic and Non-Thrombotic Disorders: Pathophysiology, Pharmacology and Therapeutics: an Update (pp. 285–296). Springer International Publishing. https://doi.org/10.1007/978-3-319-47462-5_21
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