Lijnen H R, Zamarron C, Blaber M, Winkler M E, Collen D
J Biol Chem. 1986 Jan 25;261(3):1253-8.
The mechanism of the activation of plasminogen by recombinant pro-urokinase (Rec-pro-UK), obtained by expression of the human pro-urokinase gene in Escherichia coli, was investigated in purified systems. In mixtures of Rec-pro-UK and plasminogen, both active urokinase and plasmin are quickly generated. Addition of plasmin inhibitors (aprotinin or alpha 2-antiplasmin) abolishes the conversion of Rec-pro-UK to urokinase but not the activation of plasminogen to plasmin, suggesting that Rec-pro-UK activates plasminogen directly. Human plasma competitively inhibits the activation of plasminogen by pro-urokinase with a Ki of 0.2% (v/v). This explains the relative stability of Rec-pro-UK in plasma and the lack of activation of the plasma fibrinolytic system in the absence of fibrin. The competitive inhibition by plasma is abolished by the addition of CNBr-digested fibrinogen although Rec-pro-UK has no specific affinity for fibrin. These findings suggest that the fibrin specificity of the activation of plasminogen by pro-urokinase is due to neutralization by fibrin of the competitive inhibition exerted by plasma and not to fibrin-enhanced activation of plasminogen.
通过在大肠杆菌中表达人尿激酶原基因获得的重组尿激酶原(Rec-pro-UK)激活纤溶酶原的机制,在纯化系统中进行了研究。在Rec-pro-UK和纤溶酶原的混合物中,活性尿激酶和纤溶酶都会迅速产生。添加纤溶酶抑制剂(抑肽酶或α2-抗纤溶酶)可消除Rec-pro-UK向尿激酶的转化,但不会消除纤溶酶原向纤溶酶的激活,这表明Rec-pro-UK直接激活纤溶酶原。人血浆竞争性抑制尿激酶原对纤溶酶原的激活,Ki为0.2%(v/v)。这解释了Rec-pro-UK在血浆中的相对稳定性以及在无纤维蛋白时血浆纤溶系统缺乏激活的原因。尽管Rec-pro-UK对纤维蛋白没有特异性亲和力,但添加CNBr消化的纤维蛋白原可消除血浆的竞争性抑制作用。这些发现表明,尿激酶原激活纤溶酶原的纤维蛋白特异性是由于纤维蛋白中和了血浆施加的竞争性抑制,而不是由于纤维蛋白增强了纤溶酶原的激活。