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Thrombin (Factor IIa) (EC 3.4.21.5, fibrose, thrombase, thrombofort, topical, thrombin-C, tropostasin, activated blood-coagulation factor II, E thrombin, beta-thrombin, gamma-thrombin) is a serine protease, that converts fibrinogen into strands of insoluble fibrin, as well as catalyzing many other coagulation-related reactions.
From Fibrinogen to Fibrin with the help of Thrombin and Factor XIII.. Excessive generation of fibrin due to activation of the coagulation cascade leads to thrombosis, the blockage of a vessel by an agglutination of red blood cells, platelets, polymerized fibrin and other components.
In fact, thrombin is generated by activated platelets at the initiation of the platelet plug, which in turn promotes more platelet activation. [33] Thrombin functions not only to convert fibrinogen to fibrin, it also activates Factors VIII and V and their inhibitor protein C (in the presence of thrombomodulin).
Fibrinogen is made and secreted into the blood primarily by liver hepatocyte cells. Endothelium cells are also reported to make small amounts of fibrinogen, but this fibrinogen has not been fully characterized; blood platelets and their precursors, bone marrow megakaryocytes, while once thought to make fibrinogen, are now known to take up and store but not make the glycoprotein.
Factor XIII, or fibrin stabilizing factor, is a plasma protein and zymogen. It is activated by thrombin to factor XIIIa which crosslinks fibrin in coagulation. Deficiency of XIII worsens clot stability and increases bleeding tendency. [1] Human XIII is a heterotetramer. It consists of 2 enzymatic A peptides and 2 non-enzymatic B peptides.
Coagulation activation markers are biomarkers of net activation of coagulation and fibrinolysis. [1] [2] Examples include prothrombin fragment 1+2 (F1+2), thrombin–antithrombin complex (TAT), fibrinopeptide A (FpA), fibrin monomers (FMs), plasmin-α 2-antiplasmin complex (PAP), activated protein C–protein C inhibitor (APC-PCI), and D-dimer (DD).
Plasmin breaks down fibrin into soluble parts called fibrin degradation products (FDPs). FDPs compete with thrombin, and thus slow down clot formation by preventing the conversion of fibrinogen to fibrin. This effect can be seen in the thrombin clotting time (TCT) test, which is prolonged in a person that has active fibrinolysis.
Factor Xa formed on the surface of the TF-bearing cell interacts with Factor Va to form the prothrombinase complex which generates small amounts of thrombin on the surface of TF-bearing cells. In stage 2, the amplification stage, if enough thrombin has been generated, then activation of platelets and platelet-associated cofactors occurs.