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Immunohistochemical expression of von Willebrand factor in the preeclamptic placenta
Authors:Mauro Parra-Cordero  Cleofina Bosco  Jaime González  Rodrigo Gutiérrez  Pilar Barja  Ramón Rodrigo
Affiliation:(1) Obstetrics and Gynaecology Department, University of Chile Clinical Hospital, Santiago, Chile;(2) Faculty of Medicine, Anatomy and Developmental Biology Program, Institute of Biomedical Sciences, University of Chile, Santiago, Chile;(3) Faculty of Medicine, Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, University of Chile, Independencia 1027, Casilla, 70058 Santiago 7, Chile;(4) Faculty of Medicine, Pathophysiology Program, Institute of Biomedical Sciences, University of Chile, Santiago, Chile;
Abstract:Preeclampsia is a high-prevalence systemic pregnancy disorder associated with maternal and foetal mortality. Its pathogenesis is unknown, but it is thought that oxidative stress and endothelial dysfunction may play a fundamental role. Von Willebrand factor (vWF), a marker of endothelial cell injury, can be found in different cells and zones of the placenta. To determine the differential immunoexpression of vWF at different tissue types of preeclamptic placenta and endothelial dysfunction markers at maternal serum of preeclamptic pregnancies. A case–control study was performed on a population of pregnant women with preeclampsia (n = 14), and normal pregnancies (n = 8). Placental and blood plasma samples were withdrawn at delivery. Immunohistochemical vWF expression in the placental tissue was determined. Endothelial dysfunction was assessed through plasminogen activator inhibitor (PAI) 1 and 2 ratio and vWF concentration in maternal plasma. P values less than 0.05 were considered statistically significant. Preeclamptic women showed increased plasma PAI-1/PAI-2 ratio (P < 0.05). There was diminished placental vWF expression in syncytiotrophoblast and increased in the intervillous space of preeclamptic placentas (P < 0.05). No significant differences in vWF expression were found in the villous endothelium and stroma, but it was significantly higher in maternal plasma (P < 0.05). In preeclampsia occurs endothelial damage and placental cell injury. Cell damage in syncytiotrophoblast that occurs in preeclampsia could liberate vWF from syncytiotrophoblast to the placental intervillous space, and this may have pathogenic implications.
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