Evidence map›Paper›PMID 29160127›Full record

ArticleEpigenetics2017

The fetal programming effect of prenatal smoking on Igf1r and Igf1 methylation is organ- and sex-specific.

Karolin F Meyer, Rikst Nynke Verkaik-Schakel, Wim Timens, Lester Kobzik, Torsten Plösch, Machteld N Hylkema

Open access · bronzeAbstract read
In one paragraph

Article in Epigenetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
5.3field-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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Early-life exposure to cigarette smoke primes lung function and DNA methylation changes atAmerican journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  3. Vaping and Lung Inflammation and Injury.Annual review of physiology · 2022
    Review
  4. Article
  5. Article
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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

6 authors at 1 institution in 1 country.

Karolin F Meyera Department of Pathology and Medical Biology , University of Groningen, University Medical Center Groningen , Hanzeplein 1, EA10, 9713 GZ , Groningen , The Netherlands.
Rikst Nynke Verkaik-Schakelc Department of Obstetrics and Gynaecology , University of Groningen , University Medical Center Groningen , Hanzeplein 1, 9713 GZ , Groningen , The Netherlands.
Wim Timensa Department of Pathology and Medical Biology , University of Groningen, University Medical Center Groningen , Hanzeplein 1, EA10, 9713 GZ , Groningen , The Netherlands.
Lester Kobzikd Molecular and Integrative Physiological Sciences Program, Department of Environmental Health , Harvard T. H. Chan School of Public Health , Building II Room 221, 655 Huntington Avenue, Boston , MA 02115 , USA.
Torsten Plöschc Department of Obstetrics and Gynaecology , University of Groningen , University Medical Center Groningen , Hanzeplein 1, 9713 GZ , Groningen , The Netherlands.
Machteld N Hylkemaa Department of Pathology and Medical Biology , University of Groningen, University Medical Center Groningen , Hanzeplein 1, EA10, 9713 GZ , Groningen , The Netherlands.ORCID 0000-0002-6732-8903
University Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The impact of prenatal smoke exposure (PSE) on DNA methylation has been demonstrated in blood samples from children of smoking mothers, but evidence for sex-dependent smoke-induced effects is limited. As the identified differentially methylated genes can be associated with developmental processes, and insulin-like growth factors (IGFs) play a critical role in prenatal tissue growth, we hypothesized that PSE induces fetal programming of Igf1r and Igf1. Using a mouse model of smoking during pregnancy, we show that PSE alters promoter methylation of Igf1r and Igf1 and deregulates their gene expression in lung and liver of fetal (E17.5) and neonatal (D3) mouse offspring. By further comparing female versus male, lung versus liver, or fetal versus neonatal time point, our results demonstrate that CpG site-specific aberrant methylation patterns sex-dependently vary per organ and time point. Moreover, PSE reduces gene expression of Igf1r and Igf1, dependent on organ, sex, and offspring's age. Our results indicate that PSE may be a source of organ-specific rather than general systemic fetal programming. This is exemplified here by gene promoter methylation and mRNA levels of Igf1r and Igf1, together with a sex- and organ-specific naturally established correlation of both parameters that is affected by prenatal smoke exposure. Moreover, the comparison of fetuses with neonates suggests a CpG site-dependent reversibility/persistence of PSE-induced differential methylation patterns.

Indexed as

DNA MethylationAnimalsFemaleInsulin-Like Growth Factor ILiverLungMaleMiceMice, Inbred C57BLPregnancyPrenatal Exposure Delayed EffectsPromoter Regions, GeneticReceptors, SomatomedinSex FactorsTobacco Smokinginsulin-like growth factor-1, mouseInsulin-Like Growth Factor IReceptors, SomatomedinDNA methylationepigeneticsliverlungmouseprenatalpyrosequencing

Identifiers

PMID29160127
PMCPMC5810788
OpenAlexW2770189578

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.