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. Author manuscript; available in PMC: 2011 Apr 14.
Published in final edited form as: Annu Rev Physiol. 2011 Mar 17;73:515–525. doi: 10.1146/annurev-physiol-042210-121137

Figure 1.

Figure 1

Formation of a venous clot. Venous thrombi are fibrin-rich clots that develop in the absence of gross endothelial damage. In a healthy vein (left), high levels of tissue factor pathway inhibitor (TFPI), thrombomodulin (TM), and endothelial cell protein C receptor (EPCR) maintain an antithrombotic phenotype (normal endothelium). In pathological conditions (right), elevated levels of tissue factor (TF)-positive microparticles (MPs) are present in the blood, and reduced blood flow, activation of the venous endothelium, and deposition of platelets may conspire to trigger formation of a thrombotic clot. Here we present two potential mechanisms that initiate activation of the coagulation system: (a) TF-positive MPs expressing P-selectin glycoprotein-1 (PSGL-1) dock to an activated endothelium expressing P-selectin, and (b) TF-positive MPs bind to activated platelets that adhere to the activated endothelium. In both cases, the presence of MP TF serves as a potent trigger of coagulation activation, and the continuous delivery of TF-positive MPs may enhance propagation of the thrombus.