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.
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.
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DOI：
10.1289/ehp.1408614
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发表时间：
2015-02
影响因子：
10.4
通讯作者：
Pausova Z
中科院分区：
文献类型：
--
作者：
Lee KW;Richmond R;Hu P;French L;Shin J;Bourdon C;Reischl E;Waldenberger M;Zeilinger S;Gaunt T;McArdle W;Ring S;Woodward G;Bouchard L;Gaudet D;Smith GD;Relton C;Paus T;Pausova Z
背景资料：产前暴露于母亲吸烟（产前烟雾暴露）与出生时DNA甲基化（DNAm）的改变有关。目的：我们研究这种改变是否存在从出生到青春期。研究方法：我们使用Infinium HumanMethylation 450 K BeadChip在473，395个CpG中搜索发现队列（n = 132）中青春期产前吸烟暴露相关的差异DNAm，以及复制队列（n = 447）中出生时，儿童期和青春期吸烟暴露相关的差异DNAm。结果如下：在发现队列中，我们发现MYO 1G（排名第一的CpG：cg 12803068，p = 3.3 × 10-11）和CNTNAP 2（cg 25949550，p = 4.0 × 10-9）中的5个CpG在青春期暴露和未暴露个体之间存在差异甲基化。MYO 1G和CNTNAP 2中的CpG分别与暴露于暴露的青少年和未暴露的青少年中较高和较低的DNAm相关。在复制队列中，相同的CpG在出生时、儿童期和青春期发生差异甲基化。在两个队列和所有发育时间点，差异DNAm是在相同的方向和相似的幅度，并没有改变明显的调整目前吸烟的参与者或他们的父母。此外，青少年发现队列中5个EWAS（表观全基因组关联研究）显著性CpG中的4个也是先前出生队列中差异甲基化的最高位点，该研究中观察到的CYP 1A 1、AHRR和GFI 1中CpG的差异甲基化在我们的发现队列中也很明显。结论：我们的研究结果表明，与产前母亲吸烟相关的DNA修饰可能会在暴露的后代中持续多年，至少直到青春期。引文：Lee KW，里士里士满R，Hu P，French L，Shin J，Bourdon C，Reischl E，Waldenberger M，Zeilinger S，Gaunt T，McArdle W，Ring S，Woodward G，Bouchard L，Gaudet D，Davey Smith G，Relton C，Paus T，Pausova Z. 2015.产前暴露于母亲吸烟和DNA甲基化：青少年发现样本的表观基因组关联和出生至17岁独立队列的复制环境健康展望123：193-199; http：dx.doi.org/10.1289/ehp.1408614
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. Citation: Lee KW, Richmond R, Hu P, French L, Shin J, Bourdon C, Reischl E, Waldenberger M, Zeilinger S, Gaunt T, McArdle W, Ring S, Woodward G, Bouchard L, Gaudet D, Davey Smith G, Relton C, Paus T, Pausova Z. 2015. 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. Environ Health Perspect 123:193–199; http://dx.doi.org/10.1289/ehp.1408614
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影响因子：
4.4
作者：
Bibikova, Marina;Barnes, Bret;Shen, Richard
通讯作者：
Shen, Richard
影响因子：
3.5
作者：
Anney R;Klei L;Pinto D;Almeida J;Bacchelli E;Baird G;Bolshakova N;Bölte S;Bolton PF;Bourgeron T;Brennan S;Brian J;Casey J;Conroy J;Correia C;Corsello C;Crawford EL;de Jonge M;Delorme R;Duketis E;Duque F;Estes A;Farrar P;Fernandez BA;Folstein SE;Fombonne E;Gilbert J;Gillberg C;Glessner JT;Green A;Green J;Guter SJ;Heron EA;Holt R;Howe JL;Hughes G;Hus V;Igliozzi R;Jacob S;Kenny GP;Kim C;Kolevzon A;Kustanovich V;Lajonchere CM;Lamb JA;Law-Smith M;Leboyer M;Le Couteur A;Leventhal BL;Liu XQ;Lombard F;Lord C;Lotspeich L;Lund SC;Magalhaes TR;Mantoulan C;McDougle CJ;Melhem NM;Merikangas A;Minshew NJ;Mirza GK;Munson J;Noakes C;Nygren G;Papanikolaou K;Pagnamenta AT;Parrini B;Paton T;Pickles A;Posey DJ;Poustka F;Ragoussis J;Regan R;Roberts W;Roeder K;Roge B;Rutter ML;Schlitt S;Shah N;Sheffield VC;Soorya L;Sousa I;Stoppioni V;Sykes N;Tancredi R;Thompson AP;Thomson S;Tryfon A;Tsiantis J;Van Engeland H;Vincent JB;Volkmar F;Vorstman JA;Wallace S;Wing K;Wittemeyer K;Wood S;Zurawiecki D;Zwaigenbaum L;Bailey AJ;Battaglia A;Cantor RM;Coon H;Cuccaro ML;Dawson G;Ennis S;Freitag CM;Geschwind DH;Haines JL;Klauck SM;McMahon WM;Maestrini E;Miller J;Monaco AP;Nelson SF;Nurnberger JI Jr;Oliveira G;Parr JR;Pericak-Vance MA;Piven J;Schellenberg GD;Scherer SW;Vicente AM;Wassink TH;Wijsman EM;Betancur C;Buxbaum JD;Cook EH;Gallagher L;Gill M;Hallmayer J;Paterson AD;Sutcliffe JS;Szatmari P;Vieland VJ;Hakonarson H;Devlin B
通讯作者：
Devlin B
DOI：
10.1111/j.2517-6161.1995.tb02031.x
发表时间：
1995-01-01
影响因子：
5.8
作者：
BENJAMINI, Y;HOCHBERG, Y
通讯作者：
HOCHBERG, Y
DOI：
10.1126/science.1190614
发表时间：
2010-10-29
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Feng S;Jacobsen SE;Reik W
通讯作者：
Reik W
DOI：
10.1073/pnas.1216398109
发表时间：
2012-10-30
影响因子：
11.1
作者：
Anderson, Garret R.;Galfin, Timothy;Suedhof, Thomas C.
通讯作者：
Suedhof, Thomas C.