Platelet calcium homeostasis

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Platelet calcium homeostasis Platelet calcium homeostasis. Upon receptor activation different phospholipase (PL) C isoforms hydrolyze phosphatidylinositol-4,5-bisphosphate (PIP2) to inositol-1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 releases Ca2+ from the intracellular stores in the dense tubular system (DTS)/sarcoplasmic reticulum. The transmembrane protein stromal interaction molecule 1 (STIM1) senses the reduction in Ca2+ through a decrease in Ca2+ occupancy of its EF hand domain, and then opens Orai1 Ca2+ channels in the plasma membrane, a process called store-operated calcium entry, whereas DAG mediates calcium entry through canonical transient receptor potential channel 6 (TRPC6). Additionally, a direct receptor-operated calcium (ROC) channel, P2X1, and a Na+/Ca2+ exchanger (NCX) contribute to the elevation in Ca2+ in the platelet cytoplasm. The counteracting mechanisms to replenish DTS/sarcoplasmic reticulum Ca2+ stores involve Ca2+ adenosine triphosphatases (ATPases) (SERCAs). Plasma membrane Ca2+ ATPases (PMCAs) pump Ca2+ through the plasma membrane out of the cell. ADP, adenosine diphosphate; CLEC-2, C-type lectin-like receptor 2; FcRγ, Fc receptor γ chain; FcγRIIa, Fc γ receptor IIa; GPVI, glycoprotein VI; IP3R, IP3-receptor; PI3-K, phosphatidylinositol 3-kinase; Syk, spleen tyrosine kinase. Because of controversies about the localization and role of TRPC1 in the literature, this protein is not depicted in the figure. (Adapted with permission from Varga-Szabo D, Braun A, Nieswandt B: Calcium signaling in platelets. J Thromb Haemost 7(7):1057–1066, 2009.) Source: Platelet Morphology, Biochemistry, and Function, Williams Hematology, 9e Citation: Kaushansky K, Lichtman MA, Prchal JT, Levi MM, Press OW, Burns LJ, Caligiuri M. Williams Hematology, 9e; 2015 Available at: http://accessmedicine.mhmedical.com/DownloadImage.aspx?image=/data/books/1581/kau_ch112_f003.png&sec=108078580&BookID=1581&ChapterSecID=108078506&imagename= Accessed: November 05, 2017 Copyright © 2017 McGraw-Hill Education. All rights reserved