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Epigenetic plasticity in relation to  in utero  exposures may mechanistically explain observed differences in the likelihood of developing common complex diseases including hypertension, diabetes and cardiovascular disease through the cumulative effects of subtle alterations in gene expression. Imprinted genes are essential mediators of growth and development and are characterized by differentially methylated regulatory regions (DMRs) that carry parental allele-specific methylation profiles. This theoretical 50% level of methylation provides a baseline from which endogenously- or exogenously-induced deviations in methylation can be detected. We quantified DNA methylation at imprinted gene DMRs in a large panel of human conceptal tissues, in matched buccal cell specimens collected at birth and at one year of age, and in the major cell fractions of umbilical cord blood to assess the stability of methylation at these regions. DNA methylation was measured using validated pyrosequencing assays at seven DMRs regulating the  IGF2/H19 ,  DLK1/MEG3, MEST, NNAT  and  SGCE/PEG10  imprinted domains. DMR methylation did not significantly differ for the  H19 ,  MEST  and  SGCE/PEG10  DMRs across all conceptal tissues analyzed (ANOVA p>0.10). Methylation differences at several DMRs were observed in tissues from brain ( IGF2  and  MEG3-IG  DMRs), liver ( IGF2  and  MEG3  DMRs) and placenta (both  DLK1/MEG3  DMRs and  NNAT  DMR). In most infants, methylation profiles in buccal cells at birth and at one year of age were comparable, as was methylation in the major cell fractions of umbilical cord blood. Several infants showed temporal deviations in methylation at multiple DMRs .  Similarity of inter-individual and intra-individual methylation at some, but not all of the DMRs analyzed supports the possibility that methylation of these regions can serve as useful biosensors of exposure.

Differentially Methylated Regions of Imprinted Genes in Prenatal, Perinatal and Postnatal Human Tissues