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The approximately 1 trillion platelets that circulate in an adult human are small anucleate cell fragments adapted to adhere to damaged blood vessels, to aggregate one with another, and to facilitate the generation of thrombin. These actions contribute to hemostasis by producing a platelet plug and then reinforcing the plug by the action of thrombin converting fibrinogen to fibrin strands. To accomplish these tasks, platelets have surface receptors that can bind adhesive glycoproteins; these include the GPIb/IX/V complex, which supports platelet adhesion by binding von Willebrand factor, especially under conditions of high shear, and the integrin αIIbβ3 (GPIIb/IIIa) receptor, which is platelet specific and mediates platelet aggregation by binding fibrinogen and/or von Willebrand factor. Other receptors for adhesive glycoproteins (α2β1 [GPIa/IIa], GPVI, and perhaps others for collagen; α5β1 [GPIc*/IIa] for fibronectin; and α6β1 [GPIc/IIa] for laminin) also contribute to platelet adhesion, but their precise contributions are less-well defined. Activated platelets express both surface P-selectin, which mediates interactions with leukocytes, and CD40 ligand, which activates a number of proinflammatory cells, and release chemokines and a soluble form of CD40 ligand, thus initiating an inflammatory reaction. Platelet coagulant activity results from the exposure of negatively charged phospholipids on the surface of platelets and the generation of platelet microparticles, along with release and activation of platelet factor V and perhaps exposure of specific receptors for activated coagulation factors. Platelets change shape with activation as a result of a complex reorganization of the platelet membrane skeleton and cytoskeleton. With activation, platelets undergo release of α granule, dense body, and lysosomal contents. The activation process involves a number of receptors for agonists such as adenosine diphosphate (ADP), epinephrine, thrombin, collagen, thromboxane A2, vasopressin, serotonin, platelet-activating factor, lysophosphatidic acid, sphingosine-1-phosphate, and thrombospondin, as well as several signal transduction pathways, including phosphoinositide metabolism, arachidonic acid release and conversion into thromboxane A2, and phosphorylation of a number of different target proteins. Increases in intracellular calcium result from, and further contribute to, platelet activation. Platelet activation results in a change in the conformation of the αIIbβ3 receptor, leading to high-affinity ligand binding and platelet aggregation.

Activated platelets express both surface P-selectin, which mediates interactions with leukocytes, and CD40 ligand, which activates a number of proinflammatory cells, and release chemokines and a soluble form of CD40 ligand, thus initiating an inflammatory reaction. Platelet coagulant activity results from the exposure of negatively charged phospholipids on the surface of platelets and the generation of platelet microparticles, along with release and activation of platelet factor V and perhaps exposure of specific receptors for activated coagulation factor. Platelets also act as storehouses for a variety of molecules that affect platelet function, inflammation, innate immunity, cell proliferation, vascular tone, fibrinolysis, and wound healing; these agents are actively released upon platelet activation. Other vasoactive and platelet activating substances are newly synthesized when platelets are activated. Through cooperative biochemical interactions, platelets can ...

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