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Necrotic but not apoptotic trophoblastic debris can induce endothelial cell activation but the mechanism by which endothelial cells distinguish apoptotic from necrotic debris is unclear. The NALP3 inflammasome is a pattern recognition receptor that macrophages employ to recognise “danger signals” in necrotic cell corpses. In this study, we hypothesized that endothelial cells can identify and respond...
A hallmark of preeclampsia is endothelial cell dysfunction/activation in response to “toxins” from the placenta. Necrotic trophoblastic debris (NTD) is one possible placental toxin and others include inflammatory cytokines. Calcium supplementation appears to protect “at-risk” women from developing preeclampsia by an unknown mechanism. In this study we investigate whether the addition of high levels...
The symptoms of preeclampsia are preceded by endothelial cell activation/dysfunction which is induced by a placental trigger(s) but maternal risk factor(s) also contribute to the pathogenesis of preeclampsia. In this work we have investigated the interactions of a maternal risk factor, antiphospholipid antibodies, and a placental trigger, necrotic trophoblastic debris, on the activation of endothelial...
During normal pregnancy trophoblastic debris is shed from the placenta into the maternal blood and endothelial cells may contribute to the phagocytosis of this material. Many researchers believe the majority of this trophoblastic material is apoptotic in normal pregnancy. Previously we demonstrated that phagocytosis of necrotic, but not apoptotic trophoblastic debris induced endothelial cell activation...
Preeclampsia is a major cause of pregnancy morbidity and mortality. It is hypothesised that necrotic syncytial knots and/or inflammatory factors released from the placenta into the maternal circulation are responsible for inducing the widespread endothelial cell activation that is seen in preeclampsia. Poor placental perfusion has been associated with preeclampsia, this had led to the hypothesis that...
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