دورية أكاديمية
Maternal Smoking During Pregnancy Induces Persistent Epigenetic Changes Into Adolescence, Independent of Postnatal Smoke Exposure and Is Associated With Cardiometabolic Risk
| العنوان: | Maternal Smoking During Pregnancy Induces Persistent Epigenetic Changes Into Adolescence, Independent of Postnatal Smoke Exposure and Is Associated With Cardiometabolic Risk |
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| المؤلفون: | Rauschert, S, Melton, PE, Burdge, G, Craig, JM, Godfrey, KM, Holbrook, JD, Lillycrop, K, Mori, TA, Beilin, LJ, Oddy, WH, Pennell, C, Huang, R-C |
| بيانات النشر: | FRONTIERS MEDIA SA |
| سنة النشر: | 2019 |
| المجموعة: | The University of Melbourne: Digital Repository |
| الوصف: | Background: Several studies have shown effects of current and maternal smoking during pregnancy on DNA methylation of CpG sites in newborns and later in life. Here, we hypothesized that there are long-term and persistent epigenetic effects following maternal smoking during pregnancy on adolescent offspring DNA methylation, independent of paternal and postnatal smoke exposure. Furthermore, we explored the association between DNA methylation and cardiometabolic risk factors at 17 years of age. Materials and Methods: DNA methylation was measured using the Illumina HumanMethylation450K BeadChip in whole blood from 995 participants attending the 17-year follow-up of the Raine Study. Linear mixed effects models were used to identify differential methylated CpGs, adjusting for parental smoking during pregnancy, and paternal, passive, and adolescent smoke exposure. Additional models examined the association between DNA methylation and paternal, adolescent, and passive smoking over the life course. Offspring CpGs identified were analyzed against cardiometabolic risk factors (blood pressure, triacylglycerols (TG), high-density lipoproteins cholesterol (HDL-C), and body mass index). Results: We identified 23 CpGs (genome-wide p level: 1.06 × 10-7) that were associated with maternal smoking during pregnancy, including associated genes AHRR (cancer development), FTO (obesity), CNTNAP2 (developmental processes), CYP1A1 (detoxification), MYO1G (cell signalling), and FRMD4A (nicotine dependence). A sensitivity analysis showed a dose-dependent relationship between maternal smoking and offspring methylation. These results changed little following adjustment for paternal, passive, or offspring smoking, and there were no CpGs identified that associated with these variables. Two of the 23 identified CpGs [cg00253568 (FTO) and cg00213123 (CYP1A1)] were associated with either TG (male and female), diastolic blood pressure (female only), or HDL-C (male only), after Bonferroni correction. Discussion: This study demonstrates a critical ... |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| تدمد: | 1664-8021 |
| العلاقة: | Rauschert, S., Melton, P. E., Burdge, G., Craig, J. M., Godfrey, K. M., Holbrook, J. D., Lillycrop, K., Mori, T. A., Beilin, L. J., Oddy, W. H., Pennell, C. & Huang, R. -C. (2019). Maternal Smoking During Pregnancy Induces Persistent Epigenetic Changes Into Adolescence, Independent of Postnatal Smoke Exposure and Is Associated With Cardiometabolic Risk. FRONTIERS IN GENETICS, 10 (JUL), https://doi.org/10.3389/fgene.2019.00770Test.; http://hdl.handle.net/11343/305000Test |
| الإتاحة: | https://doi.org/10.3389/fgene.2019.00770Test http://hdl.handle.net/11343/305000Test |
| حقوق: | CC BY ; https://creativecommons.org/licenses/by/4.0Test |
| رقم الانضمام: | edsbas.92E224DE |
| قاعدة البيانات: | BASE |
Full Text Finder | تدمد: | 16648021 |
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