Evidence map›Paper›PMID 24331737›Full record

ArticlePlacenta2014

Increased decidual mRNA expression levels of candidate maternal pre-eclampsia susceptibility genes are associated with clinical severity.

H E J Yong, P Murthi, A Borg, B Kalionis, E K Moses, S P Brennecke, R J Keogh

Open access · greenAbstract read
In one paragraph

Article in Placenta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 29 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Vascular mechanisms and molecular targets in hypertensive pregnancy and preeclampsia.American journal of physiology. Heart and circulatory physiology · 2020
    Review
  8. Collagen at the maternal-fetal interface in human pregnancy.International journal of biological sciences · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
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

7 authors at 2 institutions in 1 country.

H E J YongDepartment of Perinatal Medicine Pregnancy Research Centre and University of Melbourne, Department of Obstetrics and Gynaecology, Royal Women's Hospital, Locked Bag 300, Corner Grattan Street and Flemington Road, Parkville 3052, Victoria, Australia. Electronic address: ejyong@student.unimelb.edu.au.
P MurthiDepartment of Perinatal Medicine Pregnancy Research Centre and University of Melbourne, Department of Obstetrics and Gynaecology, Royal Women's Hospital, Locked Bag 300, Corner Grattan Street and Flemington Road, Parkville 3052, Victoria, Australia. Electronic address: padma@unimelb.edu.au.
A BorgDepartment of Perinatal Medicine Pregnancy Research Centre and University of Melbourne, Department of Obstetrics and Gynaecology, Royal Women's Hospital, Locked Bag 300, Corner Grattan Street and Flemington Road, Parkville 3052, Victoria, Australia. Electronic address: aj.borg@thewomens.org.au.
B KalionisDepartment of Perinatal Medicine Pregnancy Research Centre and University of Melbourne, Department of Obstetrics and Gynaecology, Royal Women's Hospital, Locked Bag 300, Corner Grattan Street and Flemington Road, Parkville 3052, Victoria, Australia. Electronic address: bill.kalionis@thewomens.org.au.
E K MosesCentre for Genetic Origins of Health and Disease, University of Western Australia, 35 Stirling Highway, Crawley 6009, Western Australia, Australia. Electronic address: eric.moses@uwa.edu.au.
S P BrenneckeDepartment of Perinatal Medicine Pregnancy Research Centre and University of Melbourne, Department of Obstetrics and Gynaecology, Royal Women's Hospital, Locked Bag 300, Corner Grattan Street and Flemington Road, Parkville 3052, Victoria, Australia. Electronic address: s.brennecke@unimelb.edu.au.
R J KeoghDepartment of Perinatal Medicine Pregnancy Research Centre and University of Melbourne, Department of Obstetrics and Gynaecology, Royal Women's Hospital, Locked Bag 300, Corner Grattan Street and Flemington Road, Parkville 3052, Victoria, Australia. Electronic address: rosemary.keogh@thewomens.org.au.
Royal Women's Hospital · AUThe University of Western Australia · AU

Funding

Identification of Pre-eclampsia Susceptibility GenesR01HD049847 · NICHD · TEXAS BIOMEDICAL RESEARCH INSTITUTE · PI MOSES, ERIC · 2006 to 2010
$3.0M
NICHD NIH HHS HD049847NICHD NIH HHS R01 HD049847
6 · The paper itself

Abstract

introductionPre-eclampsia (PE) has a familial association, with daughters of women who had PE during pregnancy having more than twice the risk of developing PE themselves. Through genome-wide linkage and genetic association studies in PE-affected families and large population samples, we previously identified the following as positional candidate maternal susceptibility genes for PE; ACVR1, INHA, INHBB, ERAP1, ERAP2, LNPEP, COL4A1 and COL4A2. The aims of this study were to determine mRNA expression levels of previously identified candidate maternal pre-eclampsia susceptibility genes from normotensive and severe PE (SPE) pregnancies and correlate mRNA expression levels with the clinical severity of SPE.

methodsThird trimester decidual tissues were collected from both normotensive (n = 21) and SPE pregnancies (n = 24) and mRNA expression levels were determined by real-time PCR. Gene expression was then correlated with several parameters of clinical severity in SPE. Statistical significance was determined by Mann-Whitney U test and Spearman's Correlation.

resultsThe data demonstrate significantly increased decidual mRNA expression levels of ACVR1, INHBB, ERAP1, ERAP2, LNPEP, COL4A1 and COL4A2 in SPE (p < 0.05). Increased mRNA expression levels of several genes - INHA, INHBB, COL4A1 and COL4A2 were correlated with earlier onset of PE and earlier delivery of the fetus (p < 0.05).

conclusionThese results suggest altered expression of maternal susceptibility genes may play roles in PE development and the course of disease severity.

Indexed as

Activin Receptors, Type IAdultCollagen Type IVDeciduaFemaleGenetic Predisposition to DiseaseHumansInhibin-beta SubunitsInhibinsPre-EclampsiaPregnancyPregnancy Trimester, ThirdRNA, MessengerActivin Receptors, Type IACVR1 protein, humanCOL4A1 protein, humanCOL4A2 protein, humanCollagen Type IVINHBB protein, humaninhibin-alpha subunitInhibin-beta SubunitsInhibinsRNA, MessengerClinical severityDeciduaGene expressionPre-eclampsiaSusceptibility genes

Identifiers

PMID24331737
PMCPMC4107207
OpenAlexW2089184512

What OpenQuestion holds

Textmetadata
LicenceTDM
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.