期刊
EPIGENOMICS
卷 8, 期 1, 页码 43-54出版社
FUTURE MEDICINE LTD
DOI: 10.2217/epi.15.91
关键词
DNA methylation; endocrine disruptors; epigenome xenoestrogens; placenta; prenatal; programming; TEXB
资金
- Spanish Ministry of Health [FIS-PI042018, FIS-PI060867, FIS-PI081151, FIS-PI09/02311, FIS-PI09/02647, FIS-PI11/00610, FIS-PI13/02429]
- Instituto de Salud Carlos III [Red INMA G03/176, CB06/02/0041]
- EU Commission [QLK4-1999-01422, QLK4-2002-00603, CONTAMED FP7-ENV-212502]
- Generalitat de Catalunya-CIRIT [1999SGR 00241]
- Fundacio La Marato de TV3
- Consejeria de Salud de la Junta de Andalucia [183/07, 0675/10]
- Diputacion Foral de Gipuzkoa [DFG06/004]
- Department of Health of the Basque Government [2005111093]
- University of Oviedo
- Fundacion Liberbank
- Fundacion Roger Torne
- FPI Grant from the Spanish Ministry of Health [BES-2009-023933]
- Formacion de Personal Investigador Grant for Short Research Stays in Foreign Institutions [BES-2009-023933]
- Institute of Health Carlos III [RD09/0076/00148]
- Regional Government of Andalusia
Background: In utero exposure to xenostrogens may modify the epigenome. We explored the association of prenatal exposure to mixtures of xenoestrogens and genome-wide placental DNA methylation. Materials & methods: Sex-specific associations between methylation changes in placental DNA by doubling the concentration of TEXB-alpha exposure were evaluated by robust multiple linear regression. Two CpG sites were selected for validation and replication in additional male born placentas. Results: No significant associations were found, although the top significant CpGs in boys were located in the LRPAP1, HAGH, PPARGC1B, KCNQ1 and KCNQ1DN genes, previously associated to birth weight, Type 2 diabetes, obesity or steroid hormone signaling. Neither technical validation nor biological replication of the results was found in boys for LRPAP and PPARGC1B. Conclusion: Some suggestive genes were differentially methylated in boys in relation to prenatal xenoestrogen exposure, but our initial findings could not be validated or replicated.
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