Evidence map›Paper›PMID 26010865›Full record

Trial reportPloS one2015

Genome-wide transcriptome directed pathway analysis of maternal pre-eclampsia susceptibility genes.

Hannah E J Yong, Phillip E Melton, Matthew P Johnson, Katy A Freed, Bill Kalionis, Padma Murthi, Shaun P Brennecke, Rosemary J Keogh, Eric K Moses

Open access · goldAbstract readClinical TrialMulticenter Study
In one paragraph

Trial report in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 2 pooled it
6.3field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 73 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Identification and Validation of DLD as a Cuproptosis-Associated Biomarker in Preeclampsia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  5. Integrated multi-omics profiling reveals the potential role of maternal systemic immune dysregulation driven by monocyte/macrophage in preeclampsia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  6. PeerJ · 2026
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  19. Maternal whole blood mRNA signatures identify women at risk of early preeclampsia: a longitudinal study.The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2021
    Article
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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 2 countries.

Hannah E J YongDepartment of Perinatal Medicine, Pregnancy Research Centre and The University of Melbourne, Department of Obstetrics and Gynaecology, The Royal Women's Hospital, Locked Bag 300, Corner Grattan Street and Flemington Road, Parkville, 3052, Victoria, Australia.
Phillip E MeltonCentre for Genetic Origins of Health and Disease, The University of Western Australia, 35 Stirling Highway, Crawley, 6009, Western Australia, Australia.
Matthew P JohnsonDepartment of Genetics, Texas Biomedical Research Institute, P.O. Box 760549, San Antonio, Texas, United States of America.
Katy A FreedDepartment of Genetics, Texas Biomedical Research Institute, P.O. Box 760549, San Antonio, Texas, United States of America.
Bill KalionisDepartment of Perinatal Medicine, Pregnancy Research Centre and The University of Melbourne, Department of Obstetrics and Gynaecology, The Royal Women's Hospital, Locked Bag 300, Corner Grattan Street and Flemington Road, Parkville, 3052, Victoria, Australia.
Padma MurthiDepartment of Perinatal Medicine, Pregnancy Research Centre and The University of Melbourne, Department of Obstetrics and Gynaecology, The Royal Women's Hospital, Locked Bag 300, Corner Grattan Street and Flemington Road, Parkville, 3052, Victoria, Australia.
Shaun P BrenneckeDepartment of Perinatal Medicine, Pregnancy Research Centre and The University of Melbourne, Department of Obstetrics and Gynaecology, The Royal Women's Hospital, Locked Bag 300, Corner Grattan Street and Flemington Road, Parkville, 3052, Victoria, Australia.
Rosemary J KeoghDepartment of Perinatal Medicine, Pregnancy Research Centre and The University of Melbourne, Department of Obstetrics and Gynaecology, The Royal Women's Hospital, Locked Bag 300, Corner Grattan Street and Flemington Road, Parkville, 3052, Victoria, Australia.
Eric K MosesCentre for Genetic Origins of Health and Disease, The University of Western Australia, 35 Stirling Highway, Crawley, 6009, Western Australia, Australia.
Royal Women's Hospital · AUTexas Biomedical Research Institute · USUniversity of Western Australia · AU

Funding

EXTRAMULAR RESEARCH FACILITIES CONSTRUCTIONC06RR017515 · NCRR · SOUTHWEST FOUNDATION FOR BIOMEDICAL RES · PI SHADE, ROBERT E · 2003 to 2003
$3.1M
Identification of Pre-eclampsia Susceptibility GenesR01HD049847 · NICHD · TEXAS BIOMEDICAL RESEARCH INSTITUTE · PI MOSES, ERIC · 2006 to 2010
$3.0M
NCRR NIH HHS C06 RR017515NCRR NIH HHS RR017515NICHD NIH HHS HD049847NICHD NIH HHS R01 HD049847
6 · The paper itself

Abstract

backgroundPreeclampsia (PE) is a serious hypertensive pregnancy disorder with a significant genetic component. Numerous genetic studies, including our own, have yielded many susceptibility genes from distinct functional groups. Additionally, transcriptome profiling of tissues at the maternal-fetal interface has likewise yielded many differentially expressed genes. Often there is little overlap between these two approaches, although genes identified in both approaches are significantly associated with PE. We have thus taken a novel integrative bioinformatics approach of analysing pathways common to the susceptibility genes and the PE transcriptome.

methodsUsing Illumina Human Ht12v4 and Wg6v3 BeadChips, transcriptome profiling was conducted on n = 65 normotensive and n = 60 PE decidua basalis tissues collected at delivery. The R software package libraries lumi and limma were used to preprocess transcript data for pathway analysis. Pathways were analysed and constructed using Pathway Studio. We examined ten candidate genes, which are from these functional groups: activin/inhibin signalling-ACVR1, ACVR1C, ACVR2A, INHA, INHBB; structural components-COL4A1, COL4A2 and M1 family aminopeptidases-ERAP1, ERAP2 and LNPEP. RESULTS/

conclusionMajor common regulators/targets of these susceptibility genes identified were AGT, IFNG, IL6, INHBA, SERPINE1, TGFB1 and VEGFA. The top two categories of pathways associated with the susceptibility genes, which were significantly altered in the PE decidual transcriptome, were apoptosis and cell signaling (p < 0.001). Thus, susceptibility genes from distinct functional groups share similar downstream pathways through common regulators/targets, some of which are altered in PE. This study contributes to a better understanding of how susceptibility genes may interact in the development of PE. With this knowledge, more targeted functional analyses of PE susceptibility genes in these key pathways can be performed to examine their contributions to the pathogenesis and severity of PE.

Indexed as

Genetic Predisposition to DiseaseGenome-Wide Association StudySignal TransductionTranscriptomeAdultFemaleHumansPre-EclampsiaPregnancy

Identifiers

PMID26010865
PMCPMC4444079
OpenAlexW1498976785

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.