The Role of Placental Trophoblast in the Pathophysiology of the Antiphospholipid Antibody Syndrome

Abstract

The antiphospholipid (aPL) antibody syndrome is characterized by severe pregnancy complications, the cause of which remains unknown. We hypothesized that the placental trophoblast is a target for aPLs. The effects of monoclonal aPLs on trophoblast function, including the invasion of JAR into matrigel-coated filters and the effects of annexin V expression on BeWo, were investigated using choriocarcinoma models. aPLs against phosphatidylserine (PS) significantly (P < 0.001) decreased the migration of JAR across the membrane. In the annexin V studies, undifferentiated BeWo did not express surface annexin V. After differentiation, BeWo expressed surface annexin V, which was removed in the presence of aPLs, resulting in increased binding of prothrombin. PS is expressed on the trophoblast surface during differentiation and invasion of extracellular matrix. Our data suggest that aPLs against PS can directly affect trophoblast function by limiting the depth of decidual invasion and by concurrently creating a procoagulant surface on trophoblast exposed to the maternal circulation.