Editing Platelet (section)

=====Platelet-coagulation factor interactions: coagulation facilitation=====
Platelet activation causes its membrane surface to become negatively charged. One of the signaling pathways turns on [[scramblase]], which moves negatively charged [[phospholipid]]s from the inner to the outer platelet membrane surface. These phospholipids then bind the [[tenase]] and [[prothrombinase]] complexes, two of the sites of interplay between platelets and the coagulation cascade. Calcium ions are essential for the binding of these coagulation factors.

In addition to interacting with vWF and fibrin, platelets interact with thrombin, Factors X, Va, VIIa, XI, IX, and prothrombin to complete formation via the coagulation cascade.<ref name=Bouchard10>{{cite journal |vauthors=Bouchard BA, Mann KG, Butenas S |title=No evidence for tissue factor on platelets |journal=Blood |volume=116 |issue=5 |pages=854–5 |date=August 2010 |pmid=20688968 |pmc=2918337 |doi=10.1182/blood-2010-05-285627}}</ref><ref>{{cite journal |vauthors=Ahmad SS, Rawala-Sheikh R, Walsh PN |title=Components and assembly of the factor X activating complex |journal=Seminars in Thrombosis and Hemostasis |volume=18 |issue=3 |pages=311–323 |date=1992 |pmid=1455249 |doi=10.1055/s-2007-1002570|s2cid=28765989 }}</ref> Human platelets do not express [[tissue factor]].<ref name=Bouchard10/> Rat platelets do express tissue factor protein and carry both tissue factor pre-mRNA and mature mRNA.<ref>{{cite journal |vauthors=Tyagi T, Ahmad S, Gupta N, Sahu A, Ahmad Y, Nair V, Chatterjee T, Bajaj N, Sengupta S, Ganju L, Singh SB, Ashraf MZ |title=Altered expression of platelet proteins and calpain activity mediate hypoxia-induced prothrombotic phenotype |journal=Blood |volume=123 |issue=8 |pages=1250–60 |date=February 2014 |pmid=24297866 |doi=10.1182/blood-2013-05-501924 |doi-access=free}}</ref>