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Prenatal exposure to maternal smoking and offspring DNA methylation across the lifecourse: findings from the Avon Longitudinal Study of Parents and Children (ALSPAC).

Richmond RC, Simpkin AJ, Woodward G, Gaunt TR, Lyttleton O, McArdle WL, Ring SM, Smith AD, Timpson NJ, Tilling K, Davey Smith G, Relton CL - Hum. Mol. Genet. (2014)

Bottom Line: Maternal smoking during pregnancy has been found to influence newborn DNA methylation in genes involved in fundamental developmental processes.An investigation of the persistence of offspring methylation associated with maternal smoking and the relative roles of the intrauterine and postnatal environment is also warranted.In cord blood, methylation at 15 CpG sites in seven gene regions (AHRR, MYO1G, GFI1, CYP1A1, CNTNAP2, KLF13 and ATP9A) was associated with maternal smoking, and a dose-dependent response was observed in relation to smoking duration and intensity.

View Article: PubMed Central - PubMed

Affiliation: MRC Integrative Epidemiology Unit (IEU), School of Social and Community Medicine, University of Bristol, Bristol BS8 2BN, UK and.

No MeSH data available.


Related in: MedlinePlus

Longitudinal trajectories of methylation at key CpG sites in the offspring of non-smokers and sustained smokers during pregnancy from birth to age 17.
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DDU739F4: Longitudinal trajectories of methylation at key CpG sites in the offspring of non-smokers and sustained smokers during pregnancy from birth to age 17.

Mentions: Longitudinal analyses were performed to investigate whether the effect of smoking on offspring methylation at birth was transient or persisted into later life. Methylation data were available for offspring in ARIES at age 7 [mean age when blood samples were taken 7.5 (SD 0.1)] and at age 17 [mean age 17.1 (SD 1.0)]. We investigated changes in methylation levels for the CpG sites that were found to be associated with maternal smoking in cord blood using multilevel modelling (Fig. 4 and Supplementary Material, Table S4). For the seven CpG sites, there were changes in methylation found during childhood, while the magnitude of change was quite small during adolescence. At CYP1A1 (cg05549655) and CNTNAP2 (cg25949550), while there was some evidence for change in methylation among the offspring of the smokers and non-smokers over time, the difference in methylation between groups persisted. Evidence for differing rates of change in methylation level between the offspring of smokers and non-smokers was found at AHRR (cg05575921), MYO1G (cg22132788), GFI1 (cg09935388) and KLF13 (cg26146569) between birth and age 7 (P-value for difference in methylation change 0.01–1 × 10−16).Figure 4.


Prenatal exposure to maternal smoking and offspring DNA methylation across the lifecourse: findings from the Avon Longitudinal Study of Parents and Children (ALSPAC).

Richmond RC, Simpkin AJ, Woodward G, Gaunt TR, Lyttleton O, McArdle WL, Ring SM, Smith AD, Timpson NJ, Tilling K, Davey Smith G, Relton CL - Hum. Mol. Genet. (2014)

Longitudinal trajectories of methylation at key CpG sites in the offspring of non-smokers and sustained smokers during pregnancy from birth to age 17.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4380069&req=5

DDU739F4: Longitudinal trajectories of methylation at key CpG sites in the offspring of non-smokers and sustained smokers during pregnancy from birth to age 17.
Mentions: Longitudinal analyses were performed to investigate whether the effect of smoking on offspring methylation at birth was transient or persisted into later life. Methylation data were available for offspring in ARIES at age 7 [mean age when blood samples were taken 7.5 (SD 0.1)] and at age 17 [mean age 17.1 (SD 1.0)]. We investigated changes in methylation levels for the CpG sites that were found to be associated with maternal smoking in cord blood using multilevel modelling (Fig. 4 and Supplementary Material, Table S4). For the seven CpG sites, there were changes in methylation found during childhood, while the magnitude of change was quite small during adolescence. At CYP1A1 (cg05549655) and CNTNAP2 (cg25949550), while there was some evidence for change in methylation among the offspring of the smokers and non-smokers over time, the difference in methylation between groups persisted. Evidence for differing rates of change in methylation level between the offspring of smokers and non-smokers was found at AHRR (cg05575921), MYO1G (cg22132788), GFI1 (cg09935388) and KLF13 (cg26146569) between birth and age 7 (P-value for difference in methylation change 0.01–1 × 10−16).Figure 4.

Bottom Line: Maternal smoking during pregnancy has been found to influence newborn DNA methylation in genes involved in fundamental developmental processes.An investigation of the persistence of offspring methylation associated with maternal smoking and the relative roles of the intrauterine and postnatal environment is also warranted.In cord blood, methylation at 15 CpG sites in seven gene regions (AHRR, MYO1G, GFI1, CYP1A1, CNTNAP2, KLF13 and ATP9A) was associated with maternal smoking, and a dose-dependent response was observed in relation to smoking duration and intensity.

View Article: PubMed Central - PubMed

Affiliation: MRC Integrative Epidemiology Unit (IEU), School of Social and Community Medicine, University of Bristol, Bristol BS8 2BN, UK and.

No MeSH data available.


Related in: MedlinePlus