Schousboe I
Blood. 1985 Nov;66(5):1086-91.
The general hypothesis for the biological function of beta 2-glycoprotein I is that it neutralizes all negatively charged macromolecules that might enter the bloodstream and diminishes unwanted activation of the blood coagulation. In the present study we report that beta 2-glycoprotein I inhibits the activation of the contact phase system of the intrinsic pathway of blood coagulation. Activation was accomplished by an ellagic acid-phospholipid suspension (Cephotest) and measured by the appearance of amidolytic activity using the chromogenic substrate H-D-Pro-Phe-Arg-p-nitroanilide (S-2302). This inhibitory effect of beta 2-glycoprotein I was observed both when Cephotest was preincubated with beta 2-glycoprotein I and when the amount of beta 2-glycoprotein I in plasma was increased by addition of beta 2-glycoprotein I to either normal or beta 2-glycoprotein I-deficient plasma. The inhibitory effect of beta 2-glycoprotein I on the contact phase activation could be one of the physiological functions of this protein.
β2-糖蛋白I生物学功能的一般假说是，它可中和所有可能进入血液循环的带负电荷的大分子，并减少不必要的血液凝固激活。在本研究中，我们报告β2-糖蛋白I可抑制内源性凝血途径接触相系统的激活。激活是通过鞣花酸-磷脂悬液（白陶土部分凝血活酶时间测定试剂）完成的，并使用发色底物H-D-脯氨酸-苯丙氨酸-精氨酸-对硝基苯胺（S-2302）通过酰胺水解活性的出现来测定。当白陶土部分凝血活酶时间测定试剂与β2-糖蛋白I预孵育时，以及当通过向正常或β2-糖蛋白I缺乏的血浆中添加β2-糖蛋白I来增加血浆中β2-糖蛋白I的量时，均观察到β2-糖蛋白I的这种抑制作用。β2-糖蛋白I对接触相激活的抑制作用可能是该蛋白的生理功能之一。
