Journal
EPIGENOMICS
Volume 9, Issue 3, Pages 267-278Publisher
FUTURE MEDICINE LTD
DOI: 10.2217/epi-2016-0132
Keywords
CpG DNA methylation; epigenetics; placenta; sexual dimorphism
Categories
Funding
- NIH [1U2COD023375, UG33OD023348, 1UG3OD023275]
- National Institute of Environmental Health Sciences [P42-ES007126, T32-ES007018, P42-ES007373, P01-ES022832]
- National Institute of Neurological Disorders and Stroke [5U01NS040069, 2R01NS040069]
- Wake Forest School of Medicine Innovation Pilot Grant
- Harold M and Mary Earnhardt Eagle Endowed Fund for Pediatric and Neonatal Research
- EPA [RD83544201]
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Aim: Sex-based differences in response to adverse prenatal environments and infant outcomes have been observed, yet the underlying mechanisms for this are unclear. The placental epigenome may be a driver of these differences. Methods: Placental DNA methylation was assessed at more than 480,000 CpG sites from male and female infants enrolled in the extremely low gestational age newborns cohort (ELGAN) and validated in a separate US-based cohort. The impact of gestational age on placental DNA methylation was further examined using the New Hampshire Birth Cohort Study for a total of n = 467 placentas. Results: A total of n = 2745 CpG sites, representing n = 587 genes, were identified as differentially methylated (p < 1 x 10(-7)). The majority (n = 582 or 99%) of these were conserved among the New Hampshire Birth Cohort. The identified genes encode proteins related to immune function, growth/transcription factor signaling and transport across cell membranes. Conclusion: These data highlight sex-dependent epigenetic patterning in the placenta and provide insight into differences in infant outcomes and responses to the perinatal environment.
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