THE ROLE OF PLACENTAL TROPHOBLAST IN THE LIPID PATHOPHYSIOLOGY OF THEANTIPHOSPHOLIPID ANTIBODY SYNDROME

PROBLEM: 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. METHOD OF STUDY: The effects of monoclonal aPLs on trophoblast functi on, including the invasion of JAR into matrigel-coated filters and the effects of annexin V expression on BeWo, were investigated using chor iocarcinoma models. RESULTS: aPLs against phosphatidylserine (PS) sign ificantly (P < 0.001) decreased the migration of JAR across the membra ne. In the annexin V studies, undifferentiated BeWo did not express su rface annexin V. After differentiation, BeWo expressed surface annexin V, which was removed in the presence of aPLs, resulting in increased binding of prothrombin. CONCLUSIONS: PS is expressed on the trophoblas t 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 concurrent ly creating a procoagulant surface on trophoblast exposed to the mater nal circulation.