Evidence map›Paper›PMID 24270552›Full record

ArticleEpigenetics2014

Postnatal stability, tissue, and time specific effects of AHRR methylation change in response to maternal smoking in pregnancy.

Boris Novakovic, Joanne Ryan, Natalie Pereira, Berin Boughton, Jeffrey M Craig, Richard Saffery

Open access · bronzeAbstract readTwin Study
In one paragraph

Article in Epigenetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
21.1field-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.

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

88 citing papers in PubMed, 127 citations in OpenAlex.

  1. Trial
  2. Vitamin C Prevents Offspring DNA Methylation Changes Associated with Maternal Smoking in Pregnancy.American journal of respiratory and critical care medicine · 2017
    Trial
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Gene-Environment Analyses Reveal Novel Genetic Candidates with Prenatal Tobacco Exposure in Relation to Risk for Childhood Acute Lymphoblastic Leukemia.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2023
    Article
  10. Early-life exposure to cigarette smoke primes lung function and DNA methylation changes atAmerican journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Epigenetics in Precision Nutrition.Journal of personalized medicine · 2022
    Review
  18. Article
  19. AhRR methylation contributes to disease progression in urothelial bladder cancer.Cancer biomarkers : section A of Disease markers · 2022
    Article
  20. Review

28 more citing papers are in PubMed but not listed here.

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

6 authors at 4 institutions in 1 country.

Boris NovakovicCancer, Disease and Developmental Epigenetics; Murdoch Childrens Research Institute; Royal Children's Hospital; Parkville, VIC Australia.
Joanne RyanCancer, Disease and Developmental Epigenetics; Murdoch Childrens Research Institute; Royal Children's Hospital; Parkville, VIC Australia; Department of Paediatrics; University of Melbourne; Parkville, VIC Australia.
Natalie PereiraMetabolomics Australia; School of Botany; The University of Melbourne; Parkville, VIC Australia.
Berin BoughtonMetabolomics Australia; School of Botany; The University of Melbourne; Parkville, VIC Australia.
Jeffrey M CraigDepartment of Paediatrics; University of Melbourne; Parkville, VIC Australia; Early Life Epigenetics; Murdoch Childrens Research Institute; Royal Children's Hospital; Parkville, VIC Australia; Department of Paediatrics; University of Melbourne; Parkville, VIC Australia.
Richard SafferyCancer, Disease and Developmental Epigenetics; Murdoch Childrens Research Institute; Royal Children's Hospital; Parkville, VIC Australia; Department of Paediatrics; University of Melbourne; Parkville, VIC Australia.
University of Melbourne · AUMurdoch Children's Research Institute · AUParks Victoria · AURoyal Children's Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The intrauterine environment has the potential to "program" the developing fetus in a way that can be potentially deleterious to later health. While in utero environmental/stochastic factors are known to influence DNA methylation profile at birth, it has been difficult to assign specific examples of epigenetic variation to specific environmental exposures. Recently, several studies have linked exposure to smoking with DNA methylation change in the aryl hydrocarbon receptor repressor (AHRR) gene in blood. This includes hypomethylation of AHRR in neonatal blood in response to maternal smoking in pregnancy. The role of AHRR as a negative regulator of pathways involved in pleiotropic responses to environmental contaminants raises the possibility that smoking-induced hypomethylation is an adaptive response to an adverse in utero environmental exposure. However, the tissue specificity of the response to maternal smoking, and the stability of the methylation changes early in life remain to be determined. In this study we analyzed AHRR methylation in three cell types-cord blood mononuclear cells (CBMCs), buccal epithelium, and placenta tissue-from newborn twins of mothers who smoked throughout pregnancy and matched controls. Further, we explored the postnatal stability of this change at 18 months. Our results confirm the previous association between maternal smoking and AHRR methylation in neonatal blood. In addition, this study expands the region of AHRR methylation altered in response to maternal smoking during pregnancy and reveals the tissue-specific nature of epigenetic responses to environmental exposures in utero. Further, the evidence for postnatal stability of smoking-induced epigenetic change supports a role for epigenetics as a mediator of long-term effects of specific in utero exposures in humans. Longitudinal analysis of further specific exposures in larger cohorts is required to examine the extent of this phenomenon in humans.

Indexed as

DNA MethylationMaternal ExposureBasic Helix-Loop-Helix ProteinsCase-Control StudiesEpigenesis, GeneticFemaleFetal BloodHumansInfant, NewbornMaternal-Fetal ExchangeOrgan SpecificityPregnancyPrenatal Exposure Delayed EffectsRepressor ProteinsSmokingAHRR protein, humanBasic Helix-Loop-Helix ProteinsRepressor ProteinsAryl hydrocarbon receptor repressor (AHRR)Cord blood mononuclear cellsDNA methylationDOHaDearly life epigeneticsintrauterine environmentsmokingtwins

Identifiers

PMID24270552
PMCPMC4053456
OpenAlexW2068396680

What OpenQuestion holds

Textmetadata
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.