Placenta · 2025
Exposure to prenatal maternal stress is associated with epigenetic age acceleration and altered cell composition in the placenta: The QF2011 Queensland Flood Study.
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Beraldo Ella O, Inkster Amy M, Peñaherrera Maria S, Price E Magda, Schuetz Johanna, Portales-Casamar Élodie, Kildea Sue, Vaillancourt Cathy, King Suzanne, Robinson Wendy P
Аннотация
BACKGROUND: Exposure to prenatal maternal stress (PNMS) in utero has been associated with several adverse perinatal outcomes, such as pre-term birth and perturbed cognitive development. As the interface between the fetal and maternal compartments during pregnancy, the placenta has been postulated to play a role in this process. We hypothesized that placental DNA methylation (DNAme) may be altered in association with natural disaster-mediated PNMS.
METHODS: Pooled placental samples from the Queensland Flood Study, or QF2011, cohort (n = 105) were processed for assessment of DNAme using the Illumina Infinium MethylationEPIC BeadChip array.
RESULTS: Overall, we did not find significant associations between placental DNAme and several stress measurements using linear modelling (FDR<0.05 and Δβ>0.03). While we found that XX placentas had slightly higher predicted cytotrophoblast to syncytiotrophoblast cell ratios than XY placentas (p = 0.01), this difference in cell ratio was not associated with PNMS exposure. However, we did observe associations between placental epigenetic age acceleration and all three types of PNMS investigated (objective hardship (QFOSS) (p = 0.03), subjective distress (COSMOSS) (p = 0.03), and maternal cognitive appraisal (CONSEQ) (p = 0.0005) scores).
CONCLUSION: The lack of large global impacts of PNMS on placental DNAme possibly indicates that the placenta can buffer moderate levels of maternal stress during pregnancy. It remains unclear what the impact of increased placental epigenetic age acceleration is on fetal development or perinatal outcomes and will require further investigation.
METHODS: Pooled placental samples from the Queensland Flood Study, or QF2011, cohort (n = 105) were processed for assessment of DNAme using the Illumina Infinium MethylationEPIC BeadChip array.
RESULTS: Overall, we did not find significant associations between placental DNAme and several stress measurements using linear modelling (FDR<0.05 and Δβ>0.03). While we found that XX placentas had slightly higher predicted cytotrophoblast to syncytiotrophoblast cell ratios than XY placentas (p = 0.01), this difference in cell ratio was not associated with PNMS exposure. However, we did observe associations between placental epigenetic age acceleration and all three types of PNMS investigated (objective hardship (QFOSS) (p = 0.03), subjective distress (COSMOSS) (p = 0.03), and maternal cognitive appraisal (CONSEQ) (p = 0.0005) scores).
CONCLUSION: The lack of large global impacts of PNMS on placental DNAme possibly indicates that the placenta can buffer moderate levels of maternal stress during pregnancy. It remains unclear what the impact of increased placental epigenetic age acceleration is on fetal development or perinatal outcomes and will require further investigation.