Henry M L, Everson B, Ratnoff O D
Department of Medicine, Case Western Reserve University, School of Medicine, Cleveland, OH.
J Lab Clin Med. 1988 May;111(5):519-23.
beta 2-Glycoprotein I (apolipoprotein H), a constituent of normal human plasma, has been shown to inhibit the generation of amidolytic activity in plasma that has been exposed to negatively charged agents. Studies with purified Hageman factor (factor XII) demonstrate that this inhibitory property is directed against the activation of Hageman factor. In this study beta 2-glycoprotein I inhibited the kaolin-induced generation of clot-promoting properties in solutions of Hageman factor. This effect was localized to an interaction between beta 2-glycoprotein I and kaolin. In contrast, once Hageman factor was activated by kaolin, its clot-promoting properties were not inhibited by beta 2-glycoprotein I. Further, beta 2-glycoprotein inhibited the generation of amidolytic activity against H-D-prolyl-L-phenylalanyl-L-arginine p-nitroanilide dihydrochloride in mixtures of Hageman factor and ellagic acid. The specificity of the action of beta 2-glycoprotein I was confirmed by its neutralization by immunoglobulin fractions of antiserums directed against this protein.
β2-糖蛋白I(载脂蛋白H)是正常人血浆的一种成分,已被证明能抑制暴露于带负电荷物质的血浆中酰胺水解活性的产生。对纯化的哈格曼因子(因子XII)的研究表明,这种抑制特性是针对哈格曼因子的激活。在本研究中,β2-糖蛋白I抑制了高岭土诱导的哈格曼因子溶液中促凝特性的产生。这种作用定位于β2-糖蛋白I与高岭土之间的相互作用。相反,一旦哈格曼因子被高岭土激活,其促凝特性就不会被β2-糖蛋白I抑制。此外,β2-糖蛋白抑制了哈格曼因子与鞣花酸混合物中对H-D-脯氨酰-L-苯丙氨酰-L-精氨酸对硝基苯胺二盐酸盐的酰胺水解活性的产生。针对该蛋白的抗血清免疫球蛋白组分对β2-糖蛋白I作用的中和作用证实了其作用的特异性。