• 1 January 1985
    • journal article
    • research article
    • Vol. 66 (5), 1086-1091
Abstract
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 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.