Document Detail

EG-VEGF controls placental growth and survival in normal and pathological pregnancies: case of fetal growth restriction (FGR).
MedLine Citation:
PMID:  22941044     Owner:  NLM     Status:  Publisher    
Identifiable causes of fetal growth restriction (FGR) account for 30 % of cases, but the remainders are idiopathic and are frequently associated with placental dysfunction. We have shown that the angiogenic factor endocrine gland-derived VEGF (EG-VEGF) and its receptors, prokineticin receptor 1 (PROKR1) and 2, (1) are abundantly expressed in human placenta, (2) are up-regulated by hypoxia, (3) control trophoblast invasion, and that EG-VEGF circulating levels are the highest during the first trimester of pregnancy, the period of important placental growth. These findings suggest that EG-VEGF/PROKR1 and 2 might be involved in normal and FGR placental development. To test this hypothesis, we used placental explants, primary trophoblast cultures, and placental and serum samples collected from FGR and age-matched control women. Our results show that (1) EG-VEGF increases trophoblast proliferation ([(3)H]-thymidine incorporation and Ki67-staining) via the homeobox-gene, HLX (2) the proliferative effect involves PROKR1 but not PROKR2, (3) EG-VEGF does not affect syncytium formation (measurement of syncytin 1 and 2 and β hCG production) (4) EG-VEGF increases the vascularization of the placental villi and insures their survival, (5) EG-VEGF, PROKR1, and PROKR2 mRNA and protein levels are significantly elevated in FGR placentas, and (6) EG-VEGF circulating levels are significantly higher in FGR patients. Altogether, our results identify EG-VEGF as a new placental growth factor acting during the first trimester of pregnancy, established its mechanism of action, and provide evidence for its deregulation in FGR. We propose that EG-VEGF/PROKR1 and 2 increases occur in FGR as a compensatory mechanism to insure proper pregnancy progress.
S Brouillet; P Murthi; P Hoffmann; A Salomon; F Sergent; P De Mazancourt; M Dakouane-Giudicelli; M N Dieudonné; P Rozenberg; D Vaiman; S Barbaux; M Benharouga; J-J Feige; N Alfaidy
Related Documents :
20463094 - Thyroid hormone early adjustment in pregnancy (the therapy) trial.
11081254 - The potential repercussions of maternal, fetal, and neonatal hypothyroxinemia on the pr...
18406314 - The systematic screening and management of hypothyroidism and hyperthyroidism during pr...
24668234 - Postnatal development of fetuses with a single umbilical artery: differences between ma...
11095924 - Does plasminogen activator inhibitor-1 (pai-1) control trophoblast invasion? a study of...
16293264 - When should signals of submission be given?-a game theory model.
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-9-2
Journal Detail:
Title:  Cellular and molecular life sciences : CMLS     Volume:  -     ISSN:  1420-9071     ISO Abbreviation:  Cell. Mol. Life Sci.     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-9-3     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9705402     Medline TA:  Cell Mol Life Sci     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Laboratoire BCI -iRTSV, Institut National de la Santé et de la Recherche Médicale U1036, Biologie du Cancer et de l'Infection, CEA Grenoble, 17, rue des Martyrs, 38054, Grenoble Cedex 9, France.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

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

Previous Document:  Cardiovascular management of septic shock in 2012.
Next Document:  Cytochrome P450–catalyzed L-tryptophan nitration in thaxtomin phytotoxin biosynthesis.