This indicates that other genomic factors, including epigenetic modifications, may be involved in predisposing some women to risk of developing PE. While there has been some success in the identification of maternal susceptibility genes for PE 9, 10, 11 they do not explain all the heritability.
Family and population studies have shown that PE has a large heritable component 4, 5, 6, 7, 8. Known risk factors for PE include first pregnancy, obesity, multiple gestation, periodontal diseases, advanced maternal age, inadequate diet, and family history 2, 3. Preeclampsia (PE) is a complex pregnancy specific disorder clinically characterized by new onset hypertension and proteinuria affecting 3-5% of pregnant women 1. This research underlines the importance for further investigation into the potential changes of differential DNA methylation in PE. We found that accelerated maternal DNAmAge is increased in women with PE in some models of epigenetic aging. When examining differences for epigenetic age acceleration between PE and normotensive women Hannum, Wu, and PhenoAge DNAmAge estimates ( p < 0.001) were significant for both epigenetic age acceleration and intrinsic acceleration models. After accounting for multiple testing and investigating differences in DNAmAge between normotensive women and women with PE, only Wu DNAmAge was significant ( p = 0.001). All seven DNAmAge measures were significantly correlated ( p < 0.001) with chronological age. No significant difference was observed for chronological age between women with PE (age = 30.53 ± 5.68) and women who had normotensive pregnancies (age = 31.76 ± 4.76). Differences between chronological age and DNAmAge and epigenetic age acceleration were investigated using t-tests. Pearson's correlation was performed to investigate associations between chronological age and DNAmAge. Three measures of DNA methylation age acceleration were calculated for all seven measures using linear regression.
#CHRONOLOGICAL AGE PEARSON SKIN#
These profiles were used to calculate seven estimates of DNAmAge and included (1) Horvath, (2) Hannum, (3) Horvath Skin and Blood, (4) Wu, (5) PhenoAge, (6) telomere length and (7) GrimAge and its surrogate measures. DNA methylation profiles were obtained using the Illumina EPIC Infinium array for analysis of genomic DNA isolated from whole blood. The case/control cohort available for study consisted of 166 women (89 with normotensive pregnancy, 77 with PE) recruited previously at the Royal Women’s Hospital in Melbourne, Australia. The aim of this study was to examine if increased maternal DNA methylation age ( DNAmAge) was shown to be accelerated in women with PE when compared to women who had normotensive pregnancies. The associations between maternal DNA methylation age and preeclampsia (PE) have not been fully assessed. Advanced biological aging, as assessed through DNA methylation markers, is associated with several complex diseases.
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