Antiphospholipid antibodies may impair factor XIIa–dependent activation of fibrinolysis in pregnancy: in vitro evidence with human endothelial cells in culture and monoclonal anticardiolipin antibodies

Abstract

The purpose of this study was to analyze the in vitro activation of the contact complex with the use of human umbilical vein endothelial cells (HUVEC) in culture and monoclonal anticardiolipin antibodies (MaCL). Cultured HUVECs were incubated with pooled plasma from third-trimester pregnant women with the addition (20 mg/mL) of MaCL with anti-beta-2 glycoprotein I activity that was obtained from patients with antiphospholipid syndrome (APS), MaCL from an individual without APS, or from a control patient with immunoglobulin M without aCL activity. Supernatants were evaluated. Activated factors XII and VII, prothrombin-fragment 1 + 2, urokinase-type plasminogen activator (UPA), and differentiating 2 chain UPA were determined. In the cultured HUVEC supernatants, the addition of MaCL increased activated factor VII and prothrombin-fragment 1 + 2, did not modify UPA, and decreased activated factor XII and differentiating 2 chain UPA, in comparison with samples with control immunoglobulin M added. The MaCL without APS activity did not change any parameter that was evaluated. MaCL with anti-beta-2 activity that was obtained from patients with APS may interfere in the activation of the contact complex during pregnancy.