Herzog EM, et al. – Here, researchers hypothesize that preeclampsia (PE) is related to altered epigenetic programming of placental and fetal tissues and that these epigenetic changes might illustrate the increased cardiovascular– and metabolic disease susceptibility in PE offspring. This investigation demonstrates differential methylation in UC–WBC and placental tissue in EOPE as compared to PTB, identifying DMPs that are related to cardiovascular system pathways. Future investigations ought to examine these loci and pathways in more detail to explain the relationship between prenatal PE exposure and the cardiovascular disease risk in offspring.

Methods

• For this research, they designed a nested case–control study.
• This study was conducted in The Rotterdam Periconceptional Cohort including 13 EOPE, 16 LOPE, and three control groups of 36 uncomplicated pregnancies, 27 normotensive fetal growth restricted and 20 normotensive preterm birth (PTB) complicated pregnancies.
• Placental tissue, newborn umbilical cord blood leucocytes (UC–WBC) and umbilical vein endothelial cells were collected and DNA methylation of cytosine–guanine dinucleotides was measured by the Illumina HumanMethylation450K BeadChip.
• An epigenome–wide analysis was performed by utilizing multiple linear regression models.

Results

• Epigenome–wide tissue–specific examination between EOPE and PTB controls uncovered 5001 mostly hypermethylated differentially methylated positions (DMPs) in UC–WBC and 869 mostly hypomethylated DMPs in placental tissue, situated in or close to genes related to cardiovascular–metabolic developmental pathways.