Author(s): Guller S
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Abstract The syncytiotrophoblast (SCT) is the outer layer of placenta which is in direct contact with maternal blood. As such it is uniquely positioned to alter maternal hemostasis and endothelial function. The syncytium is known to release anti-angiogenic factors including fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng), as well as the anti-fibrinolytic factor plasminogen activator inhibitor-1 (PAI-1). Its release of microparticles has also been suggested to play a role in regulating maternal endothelial and immune cell function. It is of note that syncytial release of the above-mentioned factors increases in preeclampsia, a major cause of maternal mortality and morbidity. In preeclampsia, hypoxia and reperfusion injury in the placenta is associated with activation of the maternal endothelium. In this review, I describe the interaction of syncytial factors with hypoxia, reactive oxygen species, and apoptosis in the pathophysiology of preeclampsia and intrauterine growth restriction. In addition, I detail the potential protective actions of placental ceruloplasmin in preeclampsia, recently described by our group to be a sensitive marker of syncytial hypoxia.
This article was published in Thromb Res
and referenced in Journal of Blood Disorders & Transfusion