|Reference : Differential expression of Vegfr-2 and its soluble form in preeclampsia.|
|Scientific journals : Article|
|Human health sciences : Reproductive medicine (gynecology, andrology, obstetrics)|
|Differential expression of Vegfr-2 and its soluble form in preeclampsia.|
|Munaut, Carine [Université de Liège - ULg > Département des sciences cliniques > Labo de biologie des tumeurs et du développement >]|
|LORQUET, Sophie [Centre Hospitalier Universitaire de Liège - CHU > > Gynécologie-Obstétrique CHR >]|
|Pequeux, Christel [Université de Liège - ULg > Département des sciences cliniques > Labo de biologie des tumeurs et du développement >]|
|Coulon, C [ > > ]|
|Le Goarant, J [ > > ]|
|CHANTRAINE, Frédéric [Centre Hospitalier Universitaire de Liège - CHU > > Gynécologie-Obstétrique CHR >]|
|Noël, Agnès [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Biologie cellulaire et moléculaire appliquée à l'homme >]|
|GOFFIN, Frédéric [Centre Hospitalier Universitaire de Liège - CHU > > Gynécologie-Obstétrique CHR >]|
|Tsatsaris, V [ > > ]|
|Subtil, D [ > > ]|
|Foidart, Jean-Michel [Université de Liège - ULg > Département des sciences cliniques > Gynécologie - Obstétrique >]|
|Public Library of Science|
|[en] 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.
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.
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.
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