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Epigenetic Regulation of Newborns' Imprinted Genes Related to Gestational Growth: Patterning by Parental Race/Ethnicity and Maternal Socioeconomic Status
Citation:
King, K., S. Murphy, AND C. Hoyo. Epigenetic Regulation of Newborns' Imprinted Genes Related to Gestational Growth: Patterning by Parental Race/Ethnicity and Maternal Socioeconomic Status. Martin Bobak and James R. Dunn (ed.), Journal of Epidemiology and Community Health. BMJ / British Medical Journal Publishing Group, London, Uk, 12(1):1-20, (2015).
Impact/Purpose:
Understanding and reducing health disparities is a key public health goal [I]. Segregation, discrimination, and historical processes result in typically worse social and environmental exposures for minorities and the disadvantaged [2, 3]. Differential exposures assorted by race/ethnicity are likely responsible for most health disparities [4], while the possible role of ancestry-linked genomic factors is not yet filly understood. Currently emerging evidence blurs the line between “nature and nurture”: social and physical risks and resources assorted by race/ethnicity and socioeconomic status (SES) may change how genes are expressed [5, 6]. Since the 2008 finding that exposure to famine in utero predicts DNA methylation and chronic disease in later life and of offspring [7, 8], epigenetic marks which regulate gene expression have been linked to such diverse outcomes as cancer, asthma, and hormonal and metabolic profiles t9- 13]. Thus epigenetics offers immense hope of explaining causal mechanisms of disease and how disparities are produced. And because many epigenetic factors are malleable, at least within specific time windows, this understanding offers prospects for prevention. Meanwhile, lift le is known about the nature and mechanisms of social patterning of epigenetic markers [14] over the lifecourse [15]. especially prior to birth. In particular, it has not been established whether social factors differentially influence distinct epigenetic marks.
Description:
BACKGROUND: Children born to parents with lower income and education are at risk for obesity and later-life risk of common chronic diseases, and epigenetics has been hypothesised to link these associations. However, epigenetic targets are unknown. We focus on a cluster of well characterised genomically imprinted genes because their monoallelic expression is regulated by DNA methylation at differentially methylated regions (DMRs), are critical in fetal growth, and DNA methylation patterns at birth have been associated with increased risk of birth weight extremes and overweight status or obesity in early childhood. METHODS: We measured DNA methylation at DMRs regulating genomically imprinted domains (IGF2/H19, DLK1/MEG3, NNAT and PLAGL1) using umbilical cord blood leucocytes from 619 infants recruited in Durham, North Carolina in 2010-2011. We examined differences in DNA methylation levels by race/ethnicity of both parents, and the role that maternal socioeconomic status (SES) may play in the association between race/ethnic epigenetic differences. RESULTS: Unadjust,ed race/ethnic differences only were evident for DMRs regulating MEG3 and IGF2; race/ethnic differences persisted in IGF2/H19 and NNAT after accounting for income and education. CONCLUSIONS: Results suggest that parental factors may not only influence DNA methylation, but also do so in ways that vary by DMR. Findings support the hypothesis that epigenetics may link the observed lower SES during the prenatal period and poor outcomes such as low birth weight; lower birth weight has previously been assooiated with adult-onset chronic diseases and conditions that include cardiovascular diseases, diabetes, obesity and some cancers.
