Mother smoking leads to methylation anomalies on 'smoke' genes in the offspring: Indelible traces of previous injuries.
Mother smoking leads to methylation anomalies on 'smoke' genes in the offspring: Indelible traces of previous injuries.
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DOI：
10.1016/j.ebiom.2018.11.022
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发表时间：
2018-12
期刊：
影响因子：
11.1
通讯作者：
Vaiman D
中科院分区：
文献类型：
--
作者：
Vaiman D
吸烟的长期后果是医学界越来越感兴趣的课题，特别是当吸烟发生在产前生活时，相关出版物的数量也在稳步增加。这是一个重要的公共卫生问题，因为例如在美国，12.3%的妇女在怀孕期间每天都吸烟。众所周知，在怀孕早期，尼古丁对人类胎儿的发育有重要影响，可能会影响不同的生理系统，如呼吸系统、心血管系统和神经系统。接触烟草衍生物还具有早期有害影响，如妊娠丧失、子宫内胎儿死亡、发病率和死亡率增加[2,3]。除了这些妊娠期后果外，长期影响也是主要关注的问题，并且积累了大量关于假定风险的流行病学数据。一个主要的科学问题是能够理解驱动这些长期影响的机制，而仅仅是流行病学分析无法做到这一点。一种强烈的新兴观点是，表观遗传学，特别是DNA甲基化，可能在胎儿对母亲吸烟行为造成的旧损伤的有机记忆中起关键作用。在2012年的一篇开创性论文中，Joubert及其同事通过对1062个脐带血dna（代表新生儿白细胞上的标记）的系统分析，证明了26个显著修饰的CpGs的存在。这些CpGs位于10个基因中，包括AHRR、CYPA1、MYO1G、CNTNAP2和gfi1[4]。这些差异是轻微的（最大约为甲基化水平的20%）。引人注目的是，这种情况非常罕见，需要强调的是，进一步的独立研究证实，在313名新生儿b[5]的相同位点上存在甲基化异常。至于长期影响，从出生到17岁都发现了相同的基因。在严格的协调协议之后，2016年进行的一项荟萃分析收集了13名新生儿和6名较大儿童的研究，证实了之前的发现。值得注意的是，基因GFI1似乎包含了基因体中10个显著修饰的CpG，在吸烟者怀孕的样本中，这些基因体的甲基化水平都有所降低。发表在本期《电子生物医学》（Parmar et al., b[8]）上的这项研究是由芬兰奥卢的Sylvain Sebert和英国帝国理工学院伦敦圣玛丽校区的Marjo-Ritta Järvelin协调的。本研究主要关注GFI1位点，并将该基因8个CpG位置的DNA甲基化异常与产前诱导联系起来
Long-term consequences of exposure to smoke is a subject of increasing interest in medicine, especially so when the exposure occurs during prenatal life and there is a steady increase in the number of related publications. It is an important Public Health issue, since for instance in the US, 12.3% of women keep smoking daily during pregnancy. At early terms (during pregnancy) it is known that nicotine has important impacts on human fetal development, potentially affecting different physiological systems such as the respiratory, the cardiovascular and the neurological system [1]. Exposure to tobacco derivatives has also early deleterious effects such as pregnancy losses, in utero fetal demise, increase morbidity and mortality [2, 3]. Beside these gestational consequences, long term effects are of major interest and abundant epidemiological data accumulates about the putative risks. A major scientific question is to be able to understand the mechanisms driving these long-term effects, inaccessible to the mere epidemiological analysis. A strong emerging idea is that epigenetics, particularly DNA methylation, might play a pivotal role in the fetal organic memory of the old injury originating from the mother smoking behavior. In a seminal paper of 2012, Joubert and coworkers demonstrated the existence of 26 significantly modified CpGs, from the systematic analysis of 1062 cord blood DNAs (representing marks on the newborn White Blood Cells). These CpGs were located in 10 genes, including AHRR, CYPA1, MYO1G, CNTNAP2 and GFI1 [4]. These differences were mild (around 20% of the methylation level at the maximum). Strikingly, and this is sufficiently rare to be stressed, further independent studies confirmed methylation anomalies at the same loci on 313 newborns [5]. About long-term effects, the same genes were found from birth until 17 years [6]. Following a drastic harmonization protocol, a metaanalysis performed in 2016 [7], that collected 13 newborn and 6 older children studies confirmed the previous findings. To note, it appeared that the gene GFI1 encompassed 10 significantly modified CpG in the gene body that all presented a decreased methylation level in samples from smoker pregnancies.The study published in this issue of EBioMedicine (Parmar et al.,[8]) was coordinated by Sylvain Sebert in Oulu in Finland and Marjo-Ritta Järvelin, in London St Mary's campus at the Imperial College in UK. The study focuses on the GFI1 locus and connects the abnormal DNA methylation at 8 CpG positions of this gene that are induced by prenatal
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影响因子：
9.8
作者：
Joubert, Bonnie R.;Felix, Janine F.;London, Stephanie J.
通讯作者：
London, Stephanie J.
影响因子：
11.1
作者：
Parmar, Priyanka;Lowry, Estelle;Sebert, Sylvain
通讯作者：
Sebert, Sylvain
母体血浆叶酸会影响新生儿的表观基因组元分析中的差异DNA甲基化。
影响因子：
16.6
作者：
Joubert BR;den Dekker HT;Felix JF;Bohlin J;Ligthart S;Beckett E;Tiemeier H;van Meurs JB;Uitterlinden AG;Hofman A;Håberg SE;Reese SE;Peters MJ;Andreassen BK;Steegers EA;Nilsen RM;Vollset SE;Midttun Ø;Ueland PM;Franco OH;Dehghan A;de Jongste JC;Wu MC;Wang T;Peddada SD;Jaddoe VW;Nystad W;Duijts L;London SJ
通讯作者：
London SJ
DOI：
10.1164/rccm.201610-2141oc
发表时间：
2017-09-15
影响因子：
24.7
作者：
Shorey-Kendrick, Lyndsey E.;McEvoy, Cindy T.;Spindel, Eliot R.
通讯作者：
Spindel, Eliot R.
影响因子：
4.4
作者：
Witt SH;Frank J;Gilles M;Lang M;Treutlein J;Streit F;Wolf IAC;Peus V;Scharnholz B;Send TS;Heilmann-Heimbach S;Sivalingam S;Dukal H;Strohmaier J;Sütterlin M;Arloth J;Laucht M;Nöthen MM;Deuschle M;Rietschel M
通讯作者：
Rietschel M