title: Differential expression of Vegfr-2 and its soluble form in preeclampsia.
abstract: 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.
  
  
  RESULTS
  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
  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.
authors.affiliation: Laboratory of Tumor and Development Biology, CHU, GIGA-Cancer, University of Liège, Liège, Belgium. c.munaut@ulg.ac.be
authors.forename: Carine
authors.initials: C
authors.lastname: Munaut
authors.forename: Sophie
authors.initials: S
authors.lastname: Lorquet
authors.forename: Christel
authors.initials: C
authors.lastname: Pequeux
authors.forename: Capucine
authors.initials: C
authors.lastname: Coulon
authors.forename: Jeanne
authors.initials: J
authors.lastname: Le Goarant
authors.forename: Frédéric
authors.initials: F
authors.lastname: Chantraine
authors.forename: Agnès
authors.initials: A
authors.lastname: Noël
authors.forename: Frédéric
authors.initials: F
authors.lastname: Goffin
authors.forename: Vassilis
authors.initials: V
authors.lastname: Tsatsaris
authors.forename: Damien
authors.initials: D
authors.lastname: Subtil
authors.forename: Jean-Michel
authors.initials: JM
authors.lastname: Foidart
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000097:blood; D000071063:Endoglin; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005602:France; D006801:Humans; D007150:Immunohistochemistry; D010920:Placenta / Q000378:metabolism*; D011225:Pre-Eclampsia / Q000097:blood*; D011247:Pregnancy; D011956:Receptors, Cell Surface / Q000097:blood; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018709:Statistics, Nonparametric; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000097:blood; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000097:blood* / Q000378:metabolism
chemical_list: D015703:Antigens, CD; C064206:ENG protein, human; D000071063:Endoglin; D011956:Receptors, Cell Surface; D040281:Vascular Endothelial Growth Factor Receptor-1; D040301:Vascular Endothelial Growth Factor Receptor-2