Publication: Expression of VEGF-C and activation of its receptors VEGFR-2 and VEGFR-3 in trophoblast
Authors
Dunk, C. ; Ahmed, A.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Placental villous development requires the
co-ordinated action of angiogenic factors on both
endothelial and trophoblast cells. Like vascular
endothelial growth factor (VEGF), VEGF-C increases
vascular permeability, stimulates endothelial cell
proliferation and migration. In the present study, we
investigated the expression of VEGF-C and its receptors
VEGFR-3 and VEGFR-2 in normal and intrauterine
growth-restricted (IUGR) placenta. Immunolocalisation
studies showed that like VEGF and VEGFR-1, VEGF-C,
VEGFR-3 and VEGFR-2 co-localised to the syncytiotrophoblast,
to cells in the maternal decidua, as well as to
the endothelium of the large placental blood vessels.
Western blot analysis demonstrated a significant
decrease in placental VEGF-C and VEGFR-3 protein
expression in severe IUGR as compared to gestationallymatched
third trimester pregnancies. Conditioned
medium from VEGF-C producing pancreatic carcinoma
(Suit-2) and endometrial epithelial (Hec-1B) cell lines
caused an increased association of the phosphorylated
extracellular signal regulated kinase (ERK) in VEGFR-3
immunoprecipitates from spontaneously transformed
first trimester trophoblast cells. VEGF121 caused dosedependant
phosphorylation of VEGFR-2 in trophoblast
cells as well as stimulating DNA svnthesis. In addition.
premixing VEGFl with Yheparin sÚlphate proteoglycan
wtentiated trooho8ast oroliferation and the association
Lf p h ~ s p hw~ith- t i~e V~E~GF R-2 receptor. VEGF165-
mediated DNA synthesis was inhibited by anti-VEGFR-
2 neutralising antibody. The results demonstrate
functional VEGFR-2 and VEGFR-3 receptors on trophoblast and suggest that the decreased expression of
VEGF-C and VEGFR-3 may contribute to the abnormai
villous development observed in IUGR placenta.
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