Platelets could also be referred to as 'cell-lets' in that they are fragments of cells rather than genuinely being cells themselves; in particular they do not contain a nucleus. Platelets are generated in the bone marrow where large cells known as megakaryocytes mature then fragment into numerous platelets. Platelets survive for around 7-10 days.
Platelets function as minute patches that stick to sites of damage to blood vessels. One of their main target adhesion molecules is von Willebrand factor, which is present on subendothelial tissues and is also expressed by endothelial cells when a blood vessel is injured.
Platelets also stick to fibrin via their glycoprotein cell surface receptor Gp IIb/IIIa.
However, their role is not simply that of a passive sticking plaster. Platelets possess a network of cytoskeletal proteins which allows them to change their shape. Activated platelets extend pseudopodia and adopt a star-like shape which facilitates adhesion. The contraction of the cytoskeletal proteins assists clumps of platelets in sealing holes in blood vessels.
The cytoskeleton of platelets enables them to detect pressure changes that are a consequence of turbulent blood flow and to enter an activated state.
The analogy with a simple sticking plaster further fials when the cytoplasm of platelets is considered. Platelet cytoplasm contains granules which promote clotting, platelet adhesion and vasoconstricion. These granules are discharged when the platelet is activated. Dense platelet granules contain ATP, ADP, calcium and serotonin; calcium is part of the coagulation cascade. Alpha granules feature some clotting factors (fibrinogen, V and XIII), vWF and assorted growth factors, all of which are integral to the formation of an effective blood clot. Thus, as well as playing a mechanical role in the formation of a blood clot platelets also discharge a chemical function.
Among the substances synthesised by platelets is thromboxane A2. Thromboxane A2 is a product of the arachidonic acid metabolic pathway and promotes vasoconstriction and platelet aggregation.
Inhibition of the generation of thromboxane A2 is the basis of the antiplatelet action of aspirin. Aspirin irreversibly inhibits the enzyme cyclo-oxygenase. Cyclo-oxygenase is essential for the creation of both thromboxane A2 and prostacyclin, the latter being a vasodilator and anticoagulant produced by endothelial cells. However, whereas endothelial cells can synthesise new cyclo-oxygenase to replace that which has been neutralised by the aspirin, platelets cannot, because they do not have a nucleus to provide the blueprint for new cyclo-oxygenase. Thus, the platelets are hamstrung and the balance in the coagulation system between thromboxane A2 and prostacyclin tips in favour of the latter.