Evidence map›Paper›PMID 37507442›Full record

ArticleScientific reports2023

Prospective epigenome and transcriptome analyses of cord and peripheral blood from preterm infants at risk of bronchopulmonary dysplasia.

Hye-Youn Cho, Xuting Wang, Michelle R Campbell, Vijayalakshmi Panduri, Silvina Coviello, Mauricio T Caballero, Brian D Bennett, Steven R Kleeberger, Fernando P Polack, Gaston Ofman and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 2 pooled it
5.4field-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

27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. LncRNA SNHG14 drives alveolar inflammation in bronchopulmonary dysplasia via DNMT3a-mediated epigenetic silencing of miR-214-3p.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  10. CCR1Frontiers in immunology · 2026
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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 6 institutions in 2 countries.

Hye-Youn Cho *Immunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, 27709, USA.
Xuting Wang *Immunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, 27709, USA.
Michelle R CampbellImmunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, 27709, USA.
Vijayalakshmi PanduriEpigenetics and Stem Cell Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, 27709, USA.
Silvina CovielloFundación INFANT, Buenos Aires, Argentina.
Mauricio T CaballeroFundación INFANT, Buenos Aires, Argentina.
Brian D BennettBiostatistics and Computational Biology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, 27709, USA.
Steven R KleebergerImmunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, 27709, USA.
Fernando P PolackFundación INFANT, Buenos Aires, Argentina.
Gaston OfmanFundación INFANT, Buenos Aires, Argentina.
Douglas A BellImmunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, Building 101, MD C3-03, 111 TW Alexander Dr., Research Triangle Park, NC, 27709, USA. bell1@niehs.nih.gov.
National Institute of Environmental Health Sciences · USNational Institutes of Health · USConsejo Nacional de Investigaciones Científicas y Técnicas · ARInfant Foundation · ARUniversity of Oklahoma Health Sciences Center · USVanderbilt University Medical Center · US

Funding

Gene Expression and MicroarraysZICES102445 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI GERRISH, KEVIN · 2009 to 2025
$31.6M
Discovery And Functional Genomics Of Environmental Response GenesZIAES100475 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BELL, DOUGLAS · 2009 to 2025
$24.4M
Discovery And Genetics Of Environmental Response GenesZ01ES100475 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BELL, DOUGLAS · 2002 to 2008
$2.9M
Intramural NIH HHS Z01 ES100475
6 · The paper itself

Abstract

Bronchopulmonary dysplasia (BPD) is a prevalent chronic lung disease of prematurity with limited treatment options. To uncover biomarkers of BPD risk, this study investigated epigenetic and transcriptomic signatures of prematurity at birth and during the neonatal period at day 14 and 28. Peripheral blood DNAs from preterm infants were applied to methylation arrays and cell-type composition was estimated by deconvolution. Covariate-adjusted robust linear regression elucidated BPD- and prolonged oxygen (≥ 14 days) exposure-associated CpGs. RNAs from cord and peripheral blood were sequenced, and differentially expressed genes (DEGs) for BPD or oxygen exposure were determined. Estimated neutrophil-lymphocyte ratios in peripheral blood at day 14 in BPD infants were significantly higher than nonBPD infants, suggesting an heightened inflammatory response in developing BPD. BPD-DEGs in cord blood indicated lymphopoiesis inhibition, altered Th1/Th2 responses, DNA damage, and organ degeneration. On day 14, BPD-associated CpGs were highly enriched in neutrophil activation, infection, and CD4 + T cell quantity, and BPD-DEGs were involved in DNA damage, cellular senescence, T cell homeostasis, and hyper-cytokinesis. On day 28, BPD-associated CpGs along with BPD-DEGs were enriched for phagocytosis, neurological disorder, and nucleotide metabolism. Oxygen supplementation markedly downregulated mitochondrial biogenesis genes and altered CpGs annotated to developmental genes. Prematurity-altered DNA methylation could cause abnormal lymphopoiesis, cellular assembly and cell cycle progression to increase BPD risk. Similar pathways between epigenome and transcriptome networks suggest coordination of the two in dysregulating leukopoiesis, adaptive immunity, and innate immunity. The results provide molecular insights into biomarkers for early detection and prevention of BPD.

Indexed as

Bronchopulmonary DysplasiaInfant, PrematureBiomarkersEpigenomeGene Expression ProfilingHumansInfantInfant, NewbornOxygenProspective StudiesBiomarkersOxygen

Identifiers

PMID37507442
PMCPMC10382533
OpenAlexW4385342140

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.