ORIGINAL PAPER Immunohistochemical expression of von Willebrand factor in the preeclamptic placenta Mauro Parra-Cordero • Cleofina Bosco • Jaime Gonza ´lez • Rodrigo Gutie ´rrez • Pilar Barja • Ramo ´n Rodrigo Received: 6 July 2011 / Accepted: 8 August 2011 / Published online: 17 August 2011 Ó Springer Science+Business Media B.V. 2011 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 immu- noexpression of vWF at different tissue types of pre- eclamptic 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 with- drawn 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 signif- icant. 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. Keywords Preeclampsia Á Placenta Á von Willebrand factor Á Syncytiotrophoblast Introduction Preeclampsia (PE) is a systemic pregnancy disorder of unknown pathogenesis and a major cause of maternal and foetal morbidity and mortality (Roberts and Cooper 2001). It affects between 0.4 and 2.8% of all pregnancies in developed countries (NHBP 1990). It is widely accepted that it origi- nates in the placenta (Redman 1991; Scott 1958; Hou et al. 2008). Deficient invasion of the spiral arteries by extravillous trophoblast cells during the first half of pregnancy is the most widely recognised predisposing factor for preeclampsia (Khong and De Wolf 1986; Hubel 1999). The normal process involves the physiological remodelling of spiral arteries from highly tortuous and thick-walled vessels into flaccid, low-resistance conduits. In preeclampsia, as a consequence Mauro Parra-Cordero, Cleofina Bosco, Jaime Gonza ´lez, Rodrigo Gutie ´rrez, Pilar Barja, Ramo ´n Rodrigo are contributed equally to this work. M. Parra-Cordero Obstetrics and Gynaecology Department, University of Chile Clinical Hospital, Santiago, Chile C. Bosco Faculty of Medicine, Anatomy and Developmental Biology Program, Institute of Biomedical Sciences, University of Chile, Santiago, Chile J. Gonza ´lez Á R. Gutie ´rrez Á R. Rodrigo (&) Faculty of Medicine, Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, University of Chile, Independencia 1027, Casilla, 70058 Santiago 7, Chile e-mail: rrodrigo@med.uchile.cl P. Barja Faculty of Medicine, Pathophysiology Program, Institute of Biomedical Sciences, University of Chile, Santiago, Chile 123 J Mol Hist (2011) 42:459–465 DOI 10.1007/s10735-011-9351-5