Evidence map›Paper›PMID 24751645›Full record

ArticleMechanisms of development2014

Novel expression of EGFL7 in placental trophoblast and endothelial cells and its implication in preeclampsia.

Lauretta A Lacko, Micol Massimiani, Jenny L Sones, Romulo Hurtado, Silvia Salvi, Sergio Ferrazzani, Robin L Davisson, Luisa Campagnolo, Heidi Stuhlmann

Open access · greenAbstract read
In one paragraph

Article in Mechanisms of development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. Observational
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  12. Review
  13. Molecular Signaling Regulating Endometrium-Blastocyst Crosstalk.International journal of molecular sciences · 2019
    Review
  14. Increased circulating levels of Epidermal Growth Factor-like Domain 7 in pregnant women affected by preeclampsia.Translational research : the journal of laboratory and clinical medicine · 2019
    Article
  15. Article
  16. Article
  17. Secondary Placental Defects inFrontiers in physiology · 2019
    Article
  18. Angiogenic factor imbalance precedes complement deposition in placentae of the BPH/5 model of preeclampsia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
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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

9 authors at 3 institutions in 3 countries.

Lauretta A LackoDepartment of Cell and Developmental Biology, Weill Cornell Medical College, 1300 York Avenue, Box 60, New York, NY 10065, United States. Electronic address: lal2018@med.cornell.edu.
Micol MassimianiDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, Via Montpellier 1, 00133 Rome, Italy. Electronic address: micol9@libero.it.
Jenny L SonesDepartment of Biomedical Sciences, College of Veterinary Medicine, Cornell University, T9-014 Veterinary Research Tower, Ithaca, NY 14853, United States. Electronic address: jll74@cornell.edu.
Romulo HurtadoDepartment of Physiology and Biophysics, Weill Cornell Medical College, 1300 York Avenue, New York, NY 10065, United States. Electronic address: roh2002@med.cornell.edu.
Silvia SalviDepartment of Gynecology and Obstetrics, Catholic University of the Sacred Heart, Largo Agostino Gemelli 8, 00168 Rome, Italy. Electronic address: silvia.salvi@edu.rm.unicatt.it.
Sergio FerrazzaniDepartment of Gynecology and Obstetrics, Catholic University of the Sacred Heart, Largo Agostino Gemelli 8, 00168 Rome, Italy. Electronic address: s.ferrazzani@rm.unicatt.it.
Robin L DavissonDepartment of Cell and Developmental Biology, Weill Cornell Medical College, 1300 York Avenue, Box 60, New York, NY 10065, United States; Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, T9-014 Veterinary Research Tower, Ithaca, NY 14853, United States. Electronic address: rld2002@med.cornell.edu.
Luisa CampagnoloDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, Via Montpellier 1, 00133 Rome, Italy. Electronic address: campagno@med.uniroma2.it.
Heidi StuhlmannDepartment of Cell and Developmental Biology, Weill Cornell Medical College, 1300 York Avenue, Box 60, New York, NY 10065, United States. Electronic address: hes2011@med.cornell.edu.
Cornell University · USUniversità Cattolica del Sacro Cuore · ITUniversity of Rome Tor Vergata · IT

Funding

Role of the brain Renin-Angiotensin Sys. in Cardiovas and Metabolic RegulationP01HL084207 · NHLBI · UNIVERSITY OF IOWA · PI SIGMUND, CURT DANIEL · 2007 to 2022
$30.2M
Training Program in Developmental BiologyT32HD060600 · NICHD · WEILL MEDICAL COLL OF CORNELL UNIV · PI BAO, ZHIRONG, STUHLMANN, HEIDI · 2010 to 2024
$3.5M
Role of Egfl7 in Vascular Development and AngiogenesisR01HL082098 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI STUHLMANN, HEIDI · 2006 to 2015
$3.3M
NHLBI NIH HHS P01 HL084207NHLBI NIH HHS R01 HL082098NICHD NIH HHS T32 HD060600
6 · The paper itself

Abstract

The mammalian placenta is the site of nutrient and gas exchange between the mother and fetus, and is comprised of two principal cell types, trophoblasts and endothelial cells. Proper placental development requires invasion and differentiation of trophoblast cells, together with coordinated fetal vasculogenesis and maternal vascular remodeling. Disruption in these processes can result in placental pathologies such as preeclampsia (PE), a disease characterized by late gestational hypertension and proteinuria. Epidermal Growth Factor Like Domain 7 (EGFL7) is a largely endothelial-restricted secreted factor that is critical for embryonic vascular development, and functions by modulating the Notch signaling pathway. However, the role of EGFL7 in placental development remains unknown. In this study, we use mouse models and human placentas to begin to understand the role of EGFL7 during normal and pathological placentation. We show that Egfl7 is expressed by the endothelium of both the maternal and fetal vasculature throughout placental development. Importantly, we uncovered a previously unknown site of EGFL7 expression in the trophoblast cell lineage, including the trophectoderm, trophoblast stem cells, and placental trophoblasts. Our results demonstrate significantly reduced Egfl7 expression in human PE placentas, concurrent with a downregulation of Notch target genes. Moreover, using the BPH/5 mouse model of PE, we show that the downregulation of Egfl7 in compromised placentas occurs prior to the onset of characteristic maternal signs of PE. Together, our results implicate Egfl7 as a possible factor in normal placental development and in the etiology of PE.

Indexed as

AdultAnimalsCalcium-Binding ProteinsCase-Control StudiesCell LineageDisease Models, AnimalDown-RegulationEGF Family of ProteinsEndothelial CellsEndothelial Growth FactorsFemaleGene Expression Regulation, DevelopmentalHumansMiceMice, Inbred C57BLPlacentaCalcium-Binding ProteinsEGF Family of ProteinsEGFL7 protein, humanEgfl7 protein, mouseEndothelial Growth FactorsProteinsReceptors, NotchRNA, MessengerEGFL7EndotheliumNotch signalingPlacentaPreeclampsiaTrophoblast

Identifiers

PMID24751645
PMCPMC4177412
OpenAlexW2040665192

What OpenQuestion holds

Textmetadata
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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.