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Hypoxia is responsible for soluble vascular endothelial growth factor receptor-1 (VEGFR-1) but not for soluble endoglin induction in villous trophoblast
Author(s) -
Carine Munaut,
Sophie Lorquet,
Christel Péqueux,
S. Blacher,
Sarah Berndt,
Françis Frankenne,
JeanMichel Foidart
Publication year - 2008
Publication title -
human reproduction
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.446
H-Index - 226
eISSN - 1460-2350
pISSN - 0268-1161
DOI - 10.1093/humrep/den114
Subject(s) - vascular endothelial growth factor , placental growth factor , endoglin , angiogenesis , trophoblast , medicine , endocrinology , hypoxia (environmental) , placenta , biology , vascular endothelial growth factor a , kinase insert domain receptor , andrology , soluble fms like tyrosine kinase 1 , chemistry , fetus , microbiology and biotechnology , vegf receptors , pregnancy , genetics , stem cell , organic chemistry , oxygen , cd34
Pre-eclampsia is a pregnancy disorder characterized by a maternal endothelial cell dysfunction associated with low levels of circulating placental growth factor (PlGF) and increased levels of total vascular endothelial growth factor (VEGF), soluble VEGF receptor-1 (sVEGFR-1), and soluble endoglin, a transforming growth factor beta1 and 3 coreceptor. Here, we tested the hypothesis that these altered levels of angiogenic cytokines and of the anti-angiogenic soluble forms of cytokine receptors could be the consequence of hypoxia.

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