Evidence map›Paper›PMID 18462791›Full record

ArticlePlacenta2008

Circulating and placental endoglin concentrations in pregnancies complicated by intrauterine growth restriction and preeclampsia.

A Jeyabalan, S McGonigal, C Gilmour, C A Hubel, A Rajakumar

Open access · greenAbstract readComparative Study
In one paragraph

Article in Placenta, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
7.6field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 74 citations in OpenAlex.

  1. Observational
  2. Review
  3. Article
  4. Article
  5. Article
  6. Transforming growth factor β signaling in uterine development and function.Journal of animal science and biotechnology · 2014
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Angiogenic factors and preeclampsia.Seminars in nephrology · 2011
    Review
  15. Article
  16. Potential markers of preeclampsia--a review.Reproductive biology and endocrinology : RB&E · 2009
    Review
  17. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

A JeyabalanDepartment of Obstetrics and Gynecology and Reproductive Sciences, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
S McGonigal
C Gilmour
C A Hubel
A Rajakumar
University of Pittsburgh · USAllegheny General Hospital · USMagee-Womens Research Institute · US

Funding

TROPHOBLAST PRODUCTS IN GENESIS OF PREECLAMPSIAP01HD030367 · NICHD · MAGEE-WOMEN'S RES INST AND FOUNDATION · PI FISHER, SUSAN J. · 1993 to 2012
$17.2M
Building Research Careers in Women's HealthK12HD043441 · NICHD · MAGEE-WOMEN'S RES INST AND FOUNDATION · PI SADOVSKY, YOEL · 2002 to 2023
$10.1M
Sources and Mechanisms of Soluble VEGFR, sFlt Expression in PreeclampsiaR03HD055219 · NICHD · MAGEE-WOMEN'S RES INST AND FOUNDATION · PI RAJAKUMAR, AUGUSTINE · 2007 to 2008
$150k
NICHD NIH HHS K12 HD043441NICHD NIH HHS K12-HD043441-04NICHD NIH HHS P01 HD030367NICHD NIH HHS P01-HD30367NICHD NIH HHS R03 HD055219NICHD NIH HHS R03-HD055219
6 · The paper itself

Abstract

Inadequate trophoblast invasion and spiral artery remodeling leading to poor placental perfusion and hypoxia are believed to underlie preeclampsia (PE) and intrauterine growth restriction (IUGR). Recent studies implicate increased circulating endoglin as a contributor to the pathogenesis of PE. The objective of this study was to determine whether placental and circulating endoglin concentrations are altered in pregnancies complicated by intrauterine growth restricted (IUGR) infants and to address the role of hypoxia on the regulation of placental endoglin. We analyzed 10 placentas each from normal pregnant (NP), PE, and IUGR subjects. Endoglin levels were 2.5-fold higher in preeclamptic placentas compared to NP (15.4+/-2.6 versus 5.7+/-1.0, p<0.01). In contrast, endoglin levels were similar in NP and IUGR placentas (5.7+/-1.0 vs 5.9+/-1.1, p=NS). Placentas from pregnancies with both PE and IUGR exhibited endoglin levels comparable to the PE group and significantly different from normotensive pregnancies with and without IUGR pregnancies (mean 14.9+/-4.0, n=9, p=0.013). Soluble endoglin concentrations in maternal plasma were comparable in NP and IUGR, but higher in women with PE (n=10 per group, p<0.05). Despite a 2-fold increase in hypoxia inducible factor, HIF-1alpha, we did not observe endoglin upregulation in NP, PE, or IUGR placental villous explants exposed to hypoxia (2% oxygen). In contrast to PE, placental or circulating endoglin is not increased in normotensive women delivering small, asymmetrically grown (IUGR) infants at term. The placentas of women with IUGR appear to be fundamentally different from PE women with respect to endoglin, despite the proposed common pathology of deficient trophoblast invasion/spiral artery remodeling and poor placental perfusion.

Indexed as

AdultAntigens, CDBirth WeightCells, CulturedCohort StudiesEndoglinFemaleFetal Growth RetardationHumansInfant, NewbornOrgan Culture TechniquesPlacentaPre-EclampsiaPregnancyReceptors, Cell SurfaceRetrospective StudiesAntigens, CDEndoglinENG protein, humanReceptors, Cell Surface

Identifiers

PMID18462791
PMCPMC2467513
OpenAlexW2036540909

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.