Antiphospholipid antibodies can specifically target placental mitochondria and induce ROS production.

Women with antiphospholipid antibodies (aPL) have increased risks of pregnancy complications, including a ten-fold increased risk of preeclampsia, which is potentially triggered by the release of placental toxins. Previously, aPL were shown to enter the outer layer of the placenta, the syncytiotrophoblast, associate with mitochondria, and alter mitochondrial function. We hypothesised that aPL may also increase mitochondrial reactive oxygen species (ROS) production, leading to cellular dysfunction and release of toxins.

Human extravillous trophoblasts bind but do not internalize antiphospholipid antibodies.

Introduction: Obstetric morbidity in women with antiphospholipid antibodies (aPLs) may reflect the adverse effects of aPLs on placental cells such as extravillous trophoblasts and the syncytiotrophoblast. Antiphospholipid antibodies may affect the syncytiotrophoblast after being internalised by members of the Low-density lipoprotein receptor (LDLR) family and the antigen of aPLs, β2 glycoprotein I.

Aim: This study aimed to determine whether aPL internalization was a mechanism by which aPLs adversely affect extravillous trophoblasts.

Antiphospholipid antibodies bind syncytiotrophoblast mitochondria and alter the proteome of extruded syncytial nuclear aggregates.

Introduction: Antiphospholipid antibodies (aPL) are autoantibodies that increase the risk of women developing the hypertensive disorder pre-eclampsia. aPL are internalised by the syncytiotrophoblast and increase extrusion of necrotic multinucleated syncytial nuclear aggregates (SNAs), which may trigger endothelial dysfunction in pre-eclampsia. The mechanisms by which aPL alter death processes in the syncytiotrophoblast leading to extrusion of SNAs are unknown.

Histopathology in the placentae of women with antiphospholipid antibodies: A systematic review of the literature.

Background: Antiphospholipid antibodies (aPLs) are a heterogenous group of autoantibodies associated with recurrent miscarriage, stillbirth, foetal growth restriction and premature birth. The cause of obstetric morbidity in women with aPLs is not completely understood. Workers have attempted to understand the role of aPLs in obstetric morbidity by investigating the histopathology of placentae from aPL-positive women.