Nawroth P P, Stern D M
J Cell Biochem. 1985;28(4):253-64. doi: 10.1002/jcb.240280403.
Although the endothelial cell is considered antithrombogenic, endothelium has recently been shown to participate in procoagulant reactions. Factor IX bound to specific endothelial cell sites can be activated by the intrinsic and extrinsic pathways of coagulation. Perturbation of endothelium results in induction of tissue factor which promotes factor VIIa-mediated activation of factors IX and X, thus initiating procoagulant events on the endothelial surface. Cell bound factor IXa, in the presence of factor VIII, promotes activation of factor X. The factor Xa formed can interact with endothelial cell factor V/Va, resulting in prothrombin activation. Thrombin then cleaves fibrinogen and a fibrin clot closely associated with the endothelial cell forms. The perturbed endothelial cell thus provides a focus of localized procoagulant events. This model suggests a simple endothelial-cell-dependent mechanism for initiation of coagulation at the site of an injured or pathological vessel.
尽管内皮细胞被认为具有抗血栓形成作用,但最近研究表明内皮也参与促凝反应。结合于特定内皮细胞位点的因子IX可通过凝血的内源性和外源性途径被激活。内皮细胞受到扰动会导致组织因子的诱导,进而促进因子VIIa介导的因子IX和X的激活,从而在内皮表面引发促凝事件。在因子VIII存在的情况下,细胞结合的因子IXa可促进因子X的激活。生成的因子Xa可与内皮细胞因子V/Va相互作用,导致凝血酶原激活。然后,凝血酶裂解纤维蛋白原,形成与内皮细胞紧密相关的纤维蛋白凝块。因此,受到扰动的内皮细胞成为局部促凝事件的焦点。该模型提示了一种简单的依赖内皮细胞的机制,可在受损或病理血管部位启动凝血过程。