Phosphatidylserine-exposed procoagulant platelet surface (PS-platelet surface)

The phosphatidylserine-exposed procoagulant platelet surface serves as a critical catalytic scaffold for the assembly of blood coagulation factor complexes. In resting platelets, phosphatidylserine (PS) is sequestered in the inner leaflet of the plasma membrane; however, upon activation by agonists like thrombin or collagen, PS is flipped to the outer leaflet. This negatively charged surface facilitates the calcium-dependent binding of vitamin K-dependent clotting factors, specifically enabling the formation of the tenase (Factors IXa/VIIIa) and prothrombinase (Factors Xa/Va) complexes. These complexes dramatically accelerate the conversion of prothrombin to thrombin, leading to fibrin clot formation. Because this surface is a focal point for pathological thrombus growth, it is a major target for anticoagulant therapies and molecular imaging of active thrombosis. Drugs interacting with this target either block the PS binding sites or inhibit the enzymatic activity of the factors localized on the membrane.

Other names

Procoagulant platelet surfaceActivated platelet membraneTenase complex assembly siteProthrombinase complex assembly sitePhosphatidylserine-expressing platelets

Drugs targeting this site typically work by either masking the exposed phosphatidylserine to prevent the assembly of the tenase and prothrombinase complexes or by directly inhibiting the activated coagulation factors (such as Xa or IIa) that are localized and concentrated on this surface.