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See detailDifferential expression of Vegfr-2 and its soluble form in preeclampsia.
Munaut, Carine ULg; LORQUET, Sophie ULg; Pequeux, Christel ULg et al

in PLoS ONE (2012), 7(3), 33475

Background: Several studies have suggested that the main features of preeclampsia (PE) are consequences of endothelial dysfunction related to excess circulating anti-angiogenic factors, most notably ... [more ▼]

Background: Several studies have suggested that the main features of preeclampsia (PE) are consequences of endothelial dysfunction related to excess circulating anti-angiogenic factors, most notably, soluble sVEGFR-1 (also known as sFlt-1) and soluble endoglin (sEng), as well as to decreased PlGF. Recently, soluble VEGF type 2 receptor (sVEGFR-2) has emerged as a crucial regulator of lymphangiogenesis. To date, however, there is a paucity of information on the changes of VEGFR-2 that occur during the clinical onset of PE. Therefore, the aim of our study was to characterize the plasma levels of VEGFR-2 in PE patients and to perform VEGFR-2 immunolocalization in placenta. METHODOLOGY/PRINCIPAL FINDINGS: By ELISA, we observed that the VEGFR-2 plasma levels were reduced during PE compared with normal gestational age matched pregnancies, whereas the VEGFR-1 and Eng plasma levels were increased. The dramatic drop in the VEGFR-1 levels shortly after delivery confirmed its placental origin. In contrast, the plasma levels of Eng and VEGFR-2 decreased only moderately during the early postpartum period. An RT-PCR analysis showed that the relative levels of VEGFR-1, sVEGFR-1 and Eng mRNA were increased in the placentas of women with severe PE. The relative levels of VEGFR-2 mRNA as well as expressing cells, were similar in both groups. We also made the novel finding that a recently described alternatively spliced VEGFR-2 mRNA variant was present at lower relative levels in the preeclamptic placentas. CONCLUSIONS/SIGNIFICANCE: Our results indicate that the plasma levels of anti-angiogenic factors, particularly VEGFR-1 and VEGFR-2, behave in different ways after delivery. The rapid decrease in plasma VEGFR-1 levels appears to be a consequence of the delivery of the placenta. The persistent circulating levels of VEGFR-2 suggest a maternal endothelial origin of this peptide. The decreased VEGFR-2 plasma levels in preeclamptic women may serve as a marker of endothelial dysfunction. [less ▲]

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See detailVascularization of the placenta and the sub-placental myometrium: feasibility and reproducibility of a three-dimensional power Doppler ultrasound quantification technique. A pilot study.
Morel, O.; Grange, G.; Fresson, J. et al

in Journal of Maternal-Fetal & Neonatal Medicine (2011), 24(2), 284-290

Objective. To assess the feasibility of placental and myometrial vascularization quantification using 3D power Doppler ultrasonography. Methods. 3D standardized acquisition was performed in the mid part ... [more ▼]

Objective. To assess the feasibility of placental and myometrial vascularization quantification using 3D power Doppler ultrasonography. Methods. 3D standardized acquisition was performed in the mid part of the utero-placental unit, once, in 38 patients undergoing normal pregnancies between 15 and 39 weeks. Vascularization parameters (VI, FI, and VFI) of placentae and myometrium were measured. Intra and inter-observer, as well as inter-acquisition reproducibility were evaluated. Results. Intra-class Correlation Coefficient of vascularization measurements were at least 0.94 for intra-observer, 0.92 for inter-observer, and 0.56 for inter-acquisition reproducibility. There was no significant difference for placental measurements for VI, FI and VFI between the second trimester and the third trimester pregnancies. Concerning the myometrium, we observed no significant difference between second and third trimester for FI. However, VI (28.090 vs. 19.374) and VFI (17.691 vs. 11.336) was significantly lower in the third trimester (p < 0.01). Conclusion. 3D quantification of placental and myometrial vascular parameters is feasible with a high intra and inter-observer reproducibility. Evaluating a potential myometrial vascular impairment appears to be as relevant as studying the placenta alone and might be of great clinical interest. We believe that this technique should therefore be evaluated in clinical observational studies. [less ▲]

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See detailStimulation of human trophoblast invasion by placental growth hormone
Lacroix, M. C.; Guibourdenche, J.; Fournier, T. et al

in Endocrinology (2005), 146(5), 2434-2444

A critical step in establishment of human pregnancy is the invasion of the uterus wall by the extravillous cytotrophoblast (EVCT), a process regulated by multiple autocrine and paracrine factors. Hormones ... [more ▼]

A critical step in establishment of human pregnancy is the invasion of the uterus wall by the extravillous cytotrophoblast (EVCT), a process regulated by multiple autocrine and paracrine factors. Hormones belonging to the GH/prolactin family are expressed at the maternofetal interface. Because they are involved in cell motility in various models, we examined the possible regulatory role of human placental GH (hPGH) in EVCT invasiveness. By using an in vitro invasion model, we found that EVCT isolated from first-trimester chorionic villi and cultured on Matrigel secreted hPGH and expressed human GH receptor ( hGHR). These data were confirmed by in situ immunohistochemistry. EVCT expressed the full-length and truncated forms of hGHR, and the Janus kinase-2/signal transducer and activator of transcription factor-5 signaling pathway was activated in EVCT by hPGH treatment. Strong hPGH and hGHR expression was observed when EVCT invaded Matrigel and moved through the pores of the filter on which they were cultured. hPGH stimulated EVCT invasiveness, and this effect was inhibited by a Janus kinase-2 inhibitor. Interestingly, hPGH was more efficient than pituitary GH in stimulating EVCT invasiveness. These results offer the first evidence for a placental role of hPGH and suggest an autocrine/ paracrine role of hPGH in the regulation of trophoblast invasion. [less ▲]

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See detailCirculating angiogenic factors and preeclampsia
Tsatsaris, V.; Goffin, Frédéric ULg; Foidart, Jean-Michel ULg

in New England Journal of Medicine [=NEJM] (2004), 350(19), 2003-2004

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See detailFetal growth restriction: a workshop report
Cetin, I.; Foidart, Jean-Michel ULg; Miozzo, M. et al

in Placenta (2004), 25(8-9), 753-757

Intrauterine growth restriction (IUGR) is associated with significantly increased perinatal morbidity and mortality as well as cardiovascular disease and glucose intolerance in adult life. A number of ... [more ▼]

Intrauterine growth restriction (IUGR) is associated with significantly increased perinatal morbidity and mortality as well as cardiovascular disease and glucose intolerance in adult life. A number of disorders from genetic to metabolic, vascular, coagulative, autoimmune, as well as infectious, can influence fetal growth by damaging the placenta, leading to IUGR as a result of many possible fetal, placental and maternal disorders. Strict definitions of IUGR and of its severity are needed in order to eventually distinguish among different phenotypes, such as gestational age at onset, degree of growth restriction and presence of hypoxia. This report explores and reviews some of the most recent developments in both clinical and basic research on intrauterine growth restriction, by seeking mechanisms that involve genetic factors, utero-placental nutrient availability and vascular growth factors. New exciting findings on the genomic imprinting defects potentially associated with IUGR, and the placental anomalies associated with the decreased nutrient transport are summarized. Moreover, recent data on angiogenic growth factors as well as new information arising from application of gene chip technologies are discussed. (C) 2004 Elsevier Ltd. All rights reserved. [less ▲]

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See detailOverexpression of the soluble vascular endothelial growth factor receptor in preeclamptic patients: Pathophysiological consequences
Tsatsaris, V.; Goffin, Frédéric ULg; Munaut, Carine ULg et al

in Journal of Clinical Endocrinology and Metabolism (2003), 88(11), 5555-5563

Several growth factors such as vascular endothelial growth factor (VEGF)-A and placental growth factor (PlGF) are involved in the placental vascular development. We investigated whether dysregulation in ... [more ▼]

Several growth factors such as vascular endothelial growth factor (VEGF)-A and placental growth factor (PlGF) are involved in the placental vascular development. We investigated whether dysregulation in the VEGF family may explain the defective uteroplacental vascularization characterizing preeclampsia. We compared pregnancies complicated by early onset severe preeclampsia or intrauterine growth retardation to normal pregnancies. Maternal plasma, placentas, and placental bed biopsies were collected. The mRNA levels of VEGF-A, PlGF, and their receptors were quantified in placentas and placental beds. Levels of VEGF-A, PlGF, and soluble VEGF receptor (VEGFR) were assessed in maternal plasma. In compromised pregnancies, elevated levels of VEGF-A and VEGFR-1 mRNAs may reflect the hypoxic status of the placenta. On contrast, the membrane-bound VEGFR-1 was decreased in the placental bed of preeclamptic patients. Preeclampsia was associated with low levels of circulating PlGF and increased levels of total VEGF-A and soluble VEGFR-1. Free VEGF-A was undetectable in maternal blood. Immunohistochemical studies revealed that VEGF-A and PlGF were localized in trophoblastic cells. Altogether, our results suggest two different pathophysiological mechanisms associated with preeclampsia. The first one is related to an overproduction of competitive soluble VEGFR-1 that may lead to suppression of VEGF-A and PlGF effects. The second one is the down-regulation of its membrane bound form (VEGFR-1) in the placental bed, which may result in the defective uteroplacental development. [less ▲]

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