Evidence map›Paper›PMID 31176514›Full record

ArticlePlacenta2019

Disrupted placental serotonin synthetic pathway and increased placental serotonin: Potential implications in the pathogenesis of human fetal growth restriction.

Suveena Ranzil, Stacey Ellery, David W Walker, Cathy Vaillancourt, Nadia Alfaidy, Alexander Bonnin, Anthony Borg, Euan M Wallace, Peter R Ebeling, Jan Jaap Erwich and 1 more

Open access · greenAbstract read
In one paragraph

Article in Placenta, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 48 citations in OpenAlex.

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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

11 authors at 8 institutions in 5 countries.

Suveena RanzilDepartment of Obstetrics and Gynaecology, Monash University, Clayton, Victoria, Australia; The Ritchie Centre, Hudson Institute of Medical Research, Clayton, Victoria, Australia.
Stacey ElleryThe Ritchie Centre, Hudson Institute of Medical Research, Clayton, Victoria, Australia.
David W WalkerRoyal Melbourne Institute of Technology University - Bundoora Campus, Melbourne, Victoria, Australia.
Cathy VaillancourtINRS-Institut Armand-Frappier, Laval, QC, Canada; BioMed Research Centre, Laval, QC, Canada Center for Interdisciplinary Research on Well-Being, Health, Society and Environment, Universite du Quebec a Montreal, Montreal, QC, Canada.
Nadia AlfaidyInstitut National de la Santé, et de la Recherche Médicale, Unité, 1036, Grenoble, France; Univ. Grenoble-Alpes, 38000, Grenoble, France; Commissariat à l'Energie Atomique (CEA), iRTSV- Biology of Cancer and infection, Grenoble, France.
Alexander BonninZilkha Neurogenetic Institute, Keck School of Medicine of University of Southern California, USA.
Anthony BorgDepartment of Maternal-Fetal Medicine, Pregnancy Research Centre, The Royal Women's Hospital, Victoria, Australia.
Euan M WallaceDepartment of Obstetrics and Gynaecology, Monash University, Clayton, Victoria, Australia; The Ritchie Centre, Hudson Institute of Medical Research, Clayton, Victoria, Australia.
Peter R EbelingDepartment of Medicine, School of Clinical Sciences, Monash University, Clayton, Victoria, Australia.
Jan Jaap ErwichDepartment of Obstetrics and Gynecology, University Medical Centre Groningen, University of Groningen, Groningen, the Netherlands.
Padma MurthiThe Ritchie Centre, Hudson Institute of Medical Research, Clayton, Victoria, Australia; Department of Maternal-Fetal Medicine, Pregnancy Research Centre, The Royal Women's Hospital, Victoria, Australia; Department of Medicine, School of Clinical Sciences, Monash University, Clayton, Victoria, Australia; Department of Obstetrics and Gynaecology, The University of Melbourne, Victoria, Australia. Electronic address: padma.murthi@monash.edu.
Hudson Institute of Medical Research · AURoyal Women's Hospital · AUInserm · FRMonash University · AURMIT University · AUUniversité du Québec à Montréal · CAUniversity Medical Center Groningen · NLUniversity of Southern California · US

Funding

Prenatal stress and antidepressants effects on offspring brain developmentR01MH106806 · NIMH · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BONNIN, ALEXANDRE · 2016 to 2020
$2.1M
NIMH NIH HHS R01 MH106806
6 · The paper itself

Abstract

objectivesPlacental insufficiency contributes to altered maternal-fetal amino acid transfer, and thereby to poor fetal growth. An important placental function is the uptake of tryptophan and its metabolism to serotonin (5-HT) and kynurenine metabolites, which are essential for fetal development. We hypothesised that placental 5-HT content will be increased in pregnancies affected with fetal growth restriction (FGR).

methodsThe components of the 5-HT synthetic pathway were determined in chorionic villus samples (CVS) from small-for gestation (SGA) and matched control collected at 10-12 weeks of human pregnancy; and in placentae from third trimester FGR and gestation-matched control pregnancies using the Fluidigm Biomarker array for mRNA expression, the activity of the enzyme TPH and 5-HT concentrations using an ELISA.

resultsGene expression for the rate limiting enzymes, TPH1 and TPH2; 5-HT transporter, SLC6A4; and 5-HT receptors HTR5A, HTR5B, HTR1D and HTR1E were detected in all CVS and third trimester placentae. No significant difference in mRNA was observed in SGA compared with control. Although there was no significant change in TPH1 mRNA, the mRNA of TPH2 and SLC6A4 was significantly decreased in FGR placentae (p < 0.05), while 5-HT receptor mRNA was significantly increased in FGR compared with control (p < 0.01). Placental TPH enzyme activity was significantly increased with a concomitant increase in the total placental 5-HT concentrations in FGR compared with control.

conclusionThis study reports differential expression and activity of the key components of the 5-HT synthetic pathway associated with the pathogenesis of FGR. Further studies are required to elucidate the functional consequences of increased placental 5-HT in FGR pregnancies.

Indexed as

AdultCase-Control StudiesFemaleFetal Growth RetardationHumansMetabolic Networks and PathwaysPlacentaPlacental InsufficiencyPregnancyPregnancy Trimester, ThirdSerotoninSerotonin Plasma Membrane Transport ProteinsTryptophan HydroxylaseUp-RegulationSerotoninSerotonin Plasma Membrane Transport ProteinsSLC6A4 protein, humanTPH1 protein, humanTPH2 protein, humanTryptophan Hydroxylase

Identifiers

PMID31176514
PMCPMC6724713
OpenAlexW2946042292

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.