Evidence map›Paper›PMID 32493484›Full record

Trial reportClinical epigenetics2020

DNA methylation loci in placenta associated with birthweight and expression of genes relevant for early development and adult diseases.

Fasil Tekola-Ayele, Xuehuo Zeng, Marion Ouidir, Tsegaselassie Workalemahu, Cuilin Zhang, Fabien Delahaye, Ronald Wapner

Registry-linked trialOpen access · goldAbstract readClinical Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Clinical epigenetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00912132 (The National Standard for Normal Fetal Growth), which is not on this map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
13.7field-weighted citation impact, top 1% 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.

NCT00912132 completednot on this map

The National Standard for Normal Fetal Growth

TypeobservationalSponsorEunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD)Ran2009 to 2013Enrolled2,802ConditionsPregnancy, Fetal Growth
3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 68 citations in OpenAlex.

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  15. Therapeutic nanoparticle safety in pregnancy: Bridging knowledge gaps with environmental insights and a translational roadmap.Journal of controlled release : official journal of the Controlled Release Society · 2025
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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

7 authors at 3 institutions in 2 countries.

Fasil Tekola-AyeleEpidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 6710B Rockledge Dr, room 3204, Bethesda, MD, 20892, USA. ayeleft@mail.nih.gov.ORCID 0000-0003-4194-9370
Xuehuo ZengDivision of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
Marion OuidirEpidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 6710B Rockledge Dr, room 3204, Bethesda, MD, 20892, USA.
Tsegaselassie WorkalemahuEpidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 6710B Rockledge Dr, room 3204, Bethesda, MD, 20892, USA.
Cuilin ZhangEpidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 6710B Rockledge Dr, room 3204, Bethesda, MD, 20892, USA.
Fabien DelahayeDepartment of Genetics, Albert Einstein College of Medicine, Bronx, New York, USA.
Ronald WapnerDepartment of Obstetrics and Gynecology, Columbia University, New York, NY, USA.
National Institutes of Health · USAlbert Einstein College of Medicine · USColumbia University · US

Funding

Genetic epidemiology of early growth and cardiometabolic diseasesZIAHD008967 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI TEKOLA-AYELE, FASIL · 2018 to 2025
$4.4M
NICHD NIH HHS HHSN275200800002INICHD NIH HHS HHSN275200800012CNICHD NIH HHS HHSN275200800013CNICHD NIH HHS HHSN275200800014CNICHD NIH HHS HHSN275200800028CNICHD NIH HHS HHSN275201000009C
6 · The paper itself

Abstract

backgroundBirthweight marks an important milestone of health across the lifespan, including cardiometabolic disease risk in later life. The placenta, a transient organ at the maternal-fetal interface, regulates fetal growth. Identifying genetic loci where DNA methylation in placenta is associated with birthweight can unravel genomic pathways that are dysregulated in aberrant fetal growth and cardiometabolic diseases in later life.

resultsWe performed placental epigenome-wide association study (EWAS) of birthweight in an ethnic diverse cohort of pregnant women (n = 301). Methylation at 15 cytosine-(phosphate)-guanine sites (CpGs) was associated with birthweight (false discovery rate (FDR) < 0.05). Methylation at four (26.7%) CpG sites was associated with placental transcript levels of 15 genes (FDR < 0.05), including genes known to be associated with adult lipid traits, inflammation and oxidative stress. Increased methylation at cg06155341 was associated with higher birthweight and lower FOSL1 expression, and lower FOSL1 expression was correlated with higher birthweight. Given the role of the FOSL1 transcription factor in regulating developmental processes at the maternal-fetal interface, epigenetic mechanisms at this locus may regulate fetal development. We demonstrated trans-tissue portability of methylation at four genes (MLLT1, PDE9A, ASAP2, and SLC20A2) implicated in birthweight by a previous study in cord blood. We also found that methylation changes known to be related to maternal underweight, preeclampsia and adult type 2 diabetes were associated with lower birthweight in placenta.

conclusionWe identified novel placental DNA methylation changes associated with birthweight. Placental epigenetic mechanisms may underlie dysregulated fetal development and early origins of adult cardiometabolic diseases. CLINICAL

trial registrationClinicalTrials.gov, NCT00912132.

Indexed as

3',5'-Cyclic-AMP PhosphodiesterasesAdultBirth WeightCardiometabolic Risk FactorsCpG IslandsDiabetes Mellitus, Type 2DNA MethylationEpigenesis, GeneticFemaleFetal BloodFetal DevelopmentFos-Related Antigen 1Gene ExpressionGTPase-Activating ProteinsHumansInfant, Low Birth Weight3',5'-Cyclic-AMP PhosphodiesterasesASAP2 protein, humanFos-Related Antigen 1GTPase-Activating ProteinsMLLT1 protein, humanNeoplasm ProteinsNuclear ProteinsPDE9A protein, humanProto-Oncogene Proteins c-fosSLC20A2 protein, humanSodium-Phosphate Cotransporter Proteins, Type IIITranscription FactorsBirthweightDevelopmental origins of health and disease (DOHaD)DNA methylationExpression quantitative trait methylation (eQTM)Fetal growthPlacentaTranscriptomics

Identifiers

PMID32493484
PMCPMC7268466
OpenAlexW3032143203

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.