Document Detail


Vasoactivity to and endogenous release of vascular endothelial growth factor in the in vitro perfused human placental lobule from pregnancies complicated by preeclampsia.
MedLine Citation:
PMID:  18845336     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Vascular endothelial growth factor (VEGF) is a potent, physiologically relevant, vasodilator of the human term fetoplacental vasculature of placental lobules from normal pregnancy. There is evidence that VEGF and its receptors are dysregulated in preeclampsia (PE). Here, we used dual perfusion of the human placental lobule to test the hypothesis that the VEGF vasodilatory effect on the fetoplacental circulation is altered in PE and examined how vascular responsiveness relates to circulating levels of free VEGF in fetal sera in this disease. Umbilical cord sera and fetal venous perfusate concentrations of free VEGF from pregnancies complicated with PE were significantly lower compared to the normal group (P<0.05 and P<0.01, respectively). There was elevated in vitro placental release of the sequestrating soluble receptor, sVEGFR-1, into the fetal-side perfusate with PE compared to the normal group (P<0.05). The umbilical sera PlGF-1 level was higher by an order of magnitude in the fetal circulation in PE compared to normal pregnancy (P<0.0001), with the placenta appearing to contribute appreciably to these levels. Placental net contribution to maternal systemic free VEGF levels appeared to be negligible in both groups. sVEGFR-1 levels were elevated in the maternal-side venous perfusate with PE compared to the normal pregnancy (P<0.01). Perfused lobules from PE pregnancy exhibited an enhanced fetoplacental vasodilatory response to exogenous VEGF (P<0.001), with a longer recovery time (P<0.05), compared to the normal control group. Extrapolation of our combined functional and biochemical data suggests that a decrease in the in vivo circulating levels of free VEGF in PE is likely to contribute to compromised fetoplacental vascular patency in this disease.
Authors:
P Brownbill; T A Mills; D F Soydemir; C P Sibley
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-10-08
Journal Detail:
Title:  Placenta     Volume:  29     ISSN:  0143-4004     ISO Abbreviation:  Placenta     Publication Date:  2008 Nov 
Date Detail:
Created Date:  2008-10-30     Completed Date:  2009-01-09     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8006349     Medline TA:  Placenta     Country:  England    
Other Details:
Languages:  eng     Pagination:  950-5     Citation Subset:  IM    
Affiliation:
Maternal and Fetal Health Research Group, School of Medical and Laboratory Sciences, University of Manchester, St. Mary's Hospital, Hathersage Road, Manchester, M13 0JH, UK. paul.brownbill@manchester.ac.uk
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MeSH Terms
Descriptor/Qualifier:
Female
Humans
Membrane Proteins / blood
Perfusion
Placenta / blood supply*,  metabolism*
Placental Circulation / physiology*
Pre-Eclampsia / metabolism*,  physiopathology*
Pregnancy
Vascular Endothelial Growth Factor A / blood*
Vasodilation / physiology
Veins / physiology
Chemical
Reg. No./Substance:
0/Membrane Proteins; 0/PIGF protein, human; 0/VEGFA protein, human; 0/Vascular Endothelial Growth Factor A

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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