Prenatal Exposure to Maternal Cigarette Smoking and DNA Methylation: Epigenome-Wide Association in a Discovery Sample of Adolescents and Replication in an Independent Cohort at Birth through 17 Years of Age.

Background: Prenatal exposure to maternal cigarette smoking (prenatal smoke exposure) had been associated with altered DNA methylation (DNAm) at birth. Objective: We examined whether such alterations are present from birth through adolescence. Methods: We used the Infinium HumanMethylation450K BeadC...

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Publicado en:Environmental Health Perspectives Vol. 123; no. 2; pp. 193 - 200
Autores principales: Lee, Ken W. K., Richmond, Rebecca, Pingzhao Hu, French, Leon, Shin, Jean, Bourdon, Celine, Reischl, Eva, Waldenberger, Melanie, Zeilinger, Sonja, Gaunt, Tom, McArdle, Wendy, Ring, Susan, Woodward, Geoff, Bouchard, Luigi, Gaudet, Daniel, Smith, George Davey, Relton, Caroline, Paus, Tomas, Pausova, Zdenka
Formato: research tables/charts Journal Article
Publicado: National Institute of Environmental Health Sciences Feb2015
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Feb2015
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      pub: National Institute of Environmental Health Sciences
      place: Research Triangle Park, North Carolina
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        atl: Prenatal Exposure to Maternal Cigarette Smoking and DNA Methylation: Epigenome-Wide Association in a Discovery Sample of Adolescents and Replication in an Independent Cohort at Birth through 17 Years of Age.
      aug:
        au:
          Lee, Ken W. K.
          Richmond, Rebecca
          Pingzhao Hu
          French, Leon
          Shin, Jean
          Bourdon, Celine
          Reischl, Eva
          Waldenberger, Melanie
          Zeilinger, Sonja
          Gaunt, Tom
          McArdle, Wendy
          Ring, Susan
          Woodward, Geoff
          Bouchard, Luigi
          Gaudet, Daniel
          Smith, George Davey
          Relton, Caroline
          Paus, Tomas
          Pausova, Zdenka
        affil: The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada.
      sug:
        subj:
          Smoking Complications
          DNA Methylation Drug Effects
          Epigenomics
          Pediatric Care
          Human
          Pregnancy
          Female
          Infant, Newborn
          Infant
          Child, Preschool
          Child
          Adolescence
          Male
          Descriptive Statistics
          Quebec
          Multiple Linear Regression
          Data Analysis Software
          Post Hoc Analysis
          Confidence Intervals
          Funding Source
          Infant, Newborn: birth-1 month
          Infant: 1-23 months
          Child, Preschool: 2-5 years
          Child: 6-12 years
          Adolescent: 13-18 years
          Female
          Male
      ab: Background: Prenatal exposure to maternal cigarette smoking (prenatal smoke exposure) had been associated with altered DNA methylation (DNAm) at birth. Objective: We examined whether such alterations are present from birth through adolescence. Methods: We used the Infinium HumanMethylation450K BeadChip to search across 473,395 CpGs for differential DNAm associated with prenatal smoke exposure during adolescence in a discovery cohort (n = 132) and at birth, during childhood, and during adolescence in a replication cohort (n = 447). Results: In the discovery cohort, we found five CpGs in MYO1G (top-ranking CpG: cg12803068, p = 3.3 × 10–11) and CNTNAP2 (cg25949550, p = 4.0 × 10–9) to be differentially methylated between exposed and nonexposed individuals during adolescence. The CpGs in MYO1G and CNTNAP2 were associated, respectively, with higher and lower DNAm in exposed versus nonexposed adolescents. The same CpGs were differentially methylated at birth, during childhood, and during adolescence in the replication cohort. In both cohorts and at all developmental time points, the differential DNAm was in the same direction and of a similar magnitude, and was not altered appreciably by adjustment for current smoking by the participants or their parents. In addition, four of the five EWAS (epigenome-wide association study)–significant CpGs in the adolescent discovery cohort were also among the top sites of differential methylation in a previous birth cohort, and differential methylation of CpGs in CYP1A1, AHRR, and GFI1 observed in that study was also evident in our discovery cohort. Conclusions: Our findings suggest that modifications of DNAm associated with prenatal maternal smoking may persist in exposed offspring for many years—at least until adolescence.
      pubtype: Academic Journal
      doctype:
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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