Editing Platelet (section)

===Aggregation===<!--Platelet aggregation redirects here-->
[[File:Platelets.jpg|thumb|Platelet clumps in a blood smear]]
Platelet aggregation begins minutes after activation, and occurs as a result of turning on the [[GPIIb/IIIa]] receptor, allowing these receptors to bind with [[von Willebrand factor|vWF]] or [[fibrinogen]].<ref name="pmid16036569"/> Each platelet has around 60,000 of these receptors.<ref>{{cite journal |vauthors=O'Halloran AM, Curtin R, O'Connor F, Dooley M, Fitzgerald A, O'Brien JK, Fitzgerald DJ, Shields DC |title=The impact of genetic variation in the region of the GPIIIa gene, on Pl expression bias and GPIIb/IIIa receptor density in platelets |journal=British Journal of Haematology |volume=132 |issue=4 |pages=494–502 |date=February 2006 |pmid=16412022 |doi=10.1111/j.1365-2141.2005.05897.x |s2cid=41983626}}</ref> When any one or more of at least nine different platelet surface receptors are turned on during activation, intraplatelet signaling pathways cause existing GpIIb/IIIa receptors to change shape — curled to straight — and thus become capable of binding.<ref name="pmid16036569"/>

Since fibrinogen is a rod-like protein with nodules on either end capable of binding GPIIb/IIIa, activated platelets with exposed GPIIb/IIIa can bind fibrinogen to aggregate. GPIIb/IIIa may also further anchor the platelets to subendothelial vWF for additional structural stabilisation.

Classically it was thought that this was the only mechanism involved in aggregation, but three other mechanisms have been identified which can initiate aggregation, depending on the velocity of blood flow (i.e. shear range).<ref>{{cite journal |vauthors=Coller BS, Cheresh DA, Asch E, Seligsohn U |title=Platelet vitronectin receptor expression differentiates Iraqi-Jewish from Arab patients with Glanzmann thrombasthenia in Israel |journal=Blood |volume=77 |issue=1 |pages=75–83 |date=January 1991 |pmid=1702031 |doi=10.1182/blood.V77.1.75.75 |doi-access=free}}</ref>