Linked Life Data

17507435

Source:http://linkedlifedata.com/resource/pubmed/id/17507435

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-8-1
pubmed:abstractText
Inadequate trophoblast invasion and spiral artery remodeling leading to poor placental perfusion are believed to underlie the pregnancy pathologies preeclampsia (PE) and intrauterine growth restriction (IUGR). The main objective of this study was to investigate hypoxia-inducible transcription factor-alpha (HIF-alpha) and downstream genes (VEGF receptor-1) Flt-1 and soluble fms-like tyrosine kinase 1 (sFlt-1) proteins in IUGR placentas. Placentas from normal pregnant (NP; n = 18), PE (n = 18), and IUGR (n = 10) patients were investigated. Normotensive patients with IUGR delivered babies at >or= 37 wk of gestation with birth weights of <10% and asymmetrical growth. HIF-1 alpha, -2 alpha, Flt-1, and sFlt-1 protein, and mRNA were assessed by Western and Northern blot analyses, respectively. The results are expressed as ratios of the densitometric values for each pair of pathologic and normal placentas, a ratio of 1.0 indicating no difference. Comparable to our earlier studies, the PE/NP ratios for HIF-1 alpha, -2 alpha, and Flt proteins were significantly increased by 50-100% (all P < 0.01 vs. 1.0). Unexpectedly, the IUGR/NP ratios for HIF-1 alpha and -2 alpha proteins were 1.03 +/- 0.07 and 0.96 +/- 0.16, respectively, and for Flt and sFlt were 1.14 +/- 0.15 and 0.95 +/- 0.12, respectively (all P = not significant vs. 1.0). Northern blot analysis revealed comparable levels of HIF-alpha mRNA in abnormal and normal placentas. In contrast to PE, HIF-alpha proteins and regulated genes are not increased in placentas from normotensive pregnant women delivering small, asymmetrically grown babies >or= 37 wk of gestation. The absence of an increase in HIF-alpha protein is not due to insufficient HIF-alpha mRNA for protein synthesis. Thus, the placentas from women with PE and late IUGR are fundamentally different at the molecular level.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0363-6119
pubmed:author
pubmed:issnType
Print
pubmed:volume
293
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
R766-74
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:17507435-Adult, pubmed-meshheading:17507435-Basic Helix-Loop-Helix Transcription Factors, pubmed-meshheading:17507435-Blood Pressure, pubmed-meshheading:17507435-Female, pubmed-meshheading:17507435-Fetal Growth Retardation, pubmed-meshheading:17507435-Humans, pubmed-meshheading:17507435-Hypoxia-Inducible Factor 1, alpha Subunit, pubmed-meshheading:17507435-Infant, Low Birth Weight, pubmed-meshheading:17507435-Infant, Newborn, pubmed-meshheading:17507435-Male, pubmed-meshheading:17507435-Membrane Proteins, pubmed-meshheading:17507435-Placenta, pubmed-meshheading:17507435-Pregnancy, pubmed-meshheading:17507435-Pregnancy Trimester, Third, pubmed-meshheading:17507435-RNA, Messenger, pubmed-meshheading:17507435-Solubility, pubmed-meshheading:17507435-Vascular Endothelial Growth Factor Receptor-1
pubmed:year
2007
pubmed:articleTitle
Placental HIF-1 alpha, HIF-2 alpha, membrane and soluble VEGF receptor-1 proteins are not increased in normotensive pregnancies complicated by late-onset intrauterine growth restriction.
pubmed:affiliation
Department of Obstetrics, Gynecology and Reproductive Sciences, Graduate School of Public Health, University of Pittsburgh School of Medicine and Magee Womens Research Institute Pittsburgh, Pittsburgh, Pennsylvania, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural