Ella O. Beraldo , Amy M. Inkster , Maria S. Peñaherrera , E Magda Price , Johanna Schuetz , Élodie Portales-Casamar , Sue Kildea , Cathy Vaillancourt , Suzanne King , Wendy P. Robinson
{"title":"暴露于产前母亲压力与表观遗传年龄加速和胎盘细胞组成改变有关:QF2011昆士兰洪水研究","authors":"Ella O. Beraldo , Amy M. Inkster , Maria S. Peñaherrera , E Magda Price , Johanna Schuetz , Élodie Portales-Casamar , Sue Kildea , Cathy Vaillancourt , Suzanne King , Wendy P. Robinson","doi":"10.1016/j.placenta.2025.09.003","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>Exposure to prenatal maternal stress (PNMS) <em>in utero</em> 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.</div></div><div><h3>Methods</h3><div>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.</div></div><div><h3>Results</h3><div>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).</div></div><div><h3>Conclusion</h3><div>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.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"171 ","pages":"Pages 16-25"},"PeriodicalIF":2.5000,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Exposure to prenatal maternal stress is associated with epigenetic age acceleration and altered cell composition in the placenta: The QF2011 Queensland Flood Study\",\"authors\":\"Ella O. Beraldo , Amy M. Inkster , Maria S. Peñaherrera , E Magda Price , Johanna Schuetz , Élodie Portales-Casamar , Sue Kildea , Cathy Vaillancourt , Suzanne King , Wendy P. Robinson\",\"doi\":\"10.1016/j.placenta.2025.09.003\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><div>Exposure to prenatal maternal stress (PNMS) <em>in utero</em> 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.</div></div><div><h3>Methods</h3><div>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.</div></div><div><h3>Results</h3><div>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).</div></div><div><h3>Conclusion</h3><div>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.</div></div>\",\"PeriodicalId\":20203,\"journal\":{\"name\":\"Placenta\",\"volume\":\"171 \",\"pages\":\"Pages 16-25\"},\"PeriodicalIF\":2.5000,\"publicationDate\":\"2025-09-03\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Placenta\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0143400425006800\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"DEVELOPMENTAL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Placenta","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0143400425006800","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"DEVELOPMENTAL BIOLOGY","Score":null,"Total":0}
Exposure to prenatal maternal stress is associated with epigenetic age acceleration and altered cell composition in the placenta: The QF2011 Queensland Flood Study
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.
期刊介绍:
Placenta publishes high-quality original articles and invited topical reviews on all aspects of human and animal placentation, and the interactions between the mother, the placenta and fetal development. Topics covered include evolution, development, genetics and epigenetics, stem cells, metabolism, transport, immunology, pathology, pharmacology, cell and molecular biology, and developmental programming. The Editors welcome studies on implantation and the endometrium, comparative placentation, the uterine and umbilical circulations, the relationship between fetal and placental development, clinical aspects of altered placental development or function, the placental membranes, the influence of paternal factors on placental development or function, and the assessment of biomarkers of placental disorders.