Abstract
Thrombomodulin(TM), is an endothelial cell surface glycoprotein that plays an important role in thromboresistance especially in microvasuculature. It forms a one to one complex with thrombin to inactivate its procoagulant property. This complex catalyzes activation of protein C and activated protein C inactivates coagulant factors Va and VIIIa in the presence of protein S. Thus, TM converts procoagulant thrombin to an anticoagulant and plays a central role in the protein C anticoagulant pathway. The physiological importance of the TM-protein C system in the prevention of thrombus formation is supported by various observations including thrombotic tendencies in patients with congenital deficiency of protein C and effective prevention of experimental thrombosis by intravenous administration of purified TM. Previous studies have shown that TM on endothelial cells is down-regulated by endotoxin, TNF or IL-1β. This loss of anticoagulant potential together with induction of tissue factor in blood coagulation by these agents is thought to be related to the hypercoagulative state of sepsis, chronic inflamation and cancer. Therefore, states of expression of TM on surfaces of endothelial cells are important in regulation of intravascular coagulation.
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