Hypoxia is responsible for soluble vascular endothelial growth factor receptor-1 (VEGFR-1) but not for soluble endoglin induction in villous trophoblast -- Munaut et al., 10.1093 humrep den114 -- Human

The Author 2008. Published by Oxford University Press on behalf of the European Nation of Human Reproduction and Embryology. All rights reserved.

For Permissions, please email: journals.permissions oxfordjournals.org Hypoxia is devolving on for soluble vascular endothelial duration element receptor-1 (VEGFR-1) however not for soluble endoglin induction in villous trophoblast Carine Munaut 1, 3, Sophie Lorquet 1, 2, Christel Pequeux 1, Sylvia Blacher 1, Sarah Berndt 1, Francis Frankenne 1 and Jean-Michel Foidart 1, 2 1 Laboratory of Tumour and Advance Biology, CRCE, CHU, GIGA, University of Liège, Tour de Pathologie (B23), Sart Tilman B-4000, Liège, Belgium 2 Branch of Obstetrics and Gynecology, Hôpital of la Citadelle, Liège, Belgium 3 Correspondance address.

Tel: +32-4-366-2453; Fax: +32-4-366-2936; E-mail: c.munaut at ulg.ac.be BACKGROUND: Pre-eclampsia is a pregnancy chaos characterized by a maternal endothelial cell dysfunction associated with low levels of circulating placental being agent (PlGF) and increased levels of complete vascular endothelial activity antecedent (VEGF), soluble VEGF receptor-1 (sVEGFR-1), and soluble endoglin, a transforming evolvement circumstance & 946;1 and 3 coreceptor.

Here, we tested the speculation that these altered levels of angiogenic cytokines and of the anti-angiogenic soluble forms of cytokine receptors could be the consequence of hypoxia.

METHODS: Typical human umbilical vein endothelial cells, immortalized cardinal trimester extravillous trophoblast cells (HTR8 SVneo) and anterior trimester placental villi explants (8-14 weeks) were used for culture under normoxia (20% O 2 ) or hypoxia (1% O 2 ). Culture media were collected for the measurement of cytokines by enzyme-linked immunosorbent assay. Total RNA was extracted for RT-PCR analysis.

RESULTS: Under hypoxia, villous trophoblast expressed higher levels of VEGF, VEGFR-1, sVEGFR-1 and VEGFR-2 mRNAs ( P « 0.001), and secreted deeper VEGF and sVEGFR-1 proteins ( P « 0.05). Additionally, sVEGFR-1 directly abolished VEGF PlGF-induced angiogenesis in the rat aortic bell assay.

CONCLUSIONS: Our results advice the hypotheses that, in pre-eclampsia, (i) overproduction of VEGF family factors by pre-eclamptic placenta is a consequence of induced hypoxia; (ii) overproduction of sVEGFR-1 by hypoxic villous trophoblast accounts for maternal unpaid VEGF depletion; (iii) low circulating continuous of free of charge PlGF is not particular related to sVEGFR-1 overproduction, on the other hand besides to hypoxia-induced mRNA down-regulation; (iv) Eng is not modulated by hypoxia.

Principal words: hypoxic trophoblast vascular endothelial vitality belongings receptor-1 soluble endoglin pre-eclampsia pregnancy Submitted on Nov 22, 2007; resubmitted on Feb 25, 2008; universal on Hike 10, 2008. CiteULike Connotea Del.icio.us What's this? Disclaimer: Please message that abstracts for content published before 1996 were created fini digital scanning and may since not prerrogative replicate the issue of the elementary print issues.