抄録
Vascular endothelial cells (VECs) and blood components coordinate to maintain blood fluidity and flow. High expressions of anti-coagulatory factors as well as profibrinolytic proteins are essential for VECs to prevent thrombus formation. Heparan sulphate, a cofactor for anti-thrombin, and thrombomodulin, a modifier of thrombin's function from coagulatory to anti-coagulatory, as well as prostacyclin and NO are representative anti-coagulatory factors. Tissue plasminogen activator (tPA) is the representative of pro-fibrinolytic protein. Impairment of these function and/or expression of other thrombogenic factors, in turn, initiates thrombotic disorders, which are frequently seen in inflammation, mental stress, and metabolic syndrome. Tissue factor, an initiator of coagulation, and PA inhibitor 1 (PAI-1), a specific tPA inhibitor, are known to be expressed in VECs only under pathological conditions and trigger thrombosis. In blood, several factors including fibrinogen and PAI-1 also increase under certain pathological condition, which increases the risk for thrombosis. In this symposium, we discuss how VECs and blood components function to maintain blood fluidity, and how thrombosis event is initiated when these mechanisms are impaired [J Physiol Sci. 2008;58 Suppl:S39]
