Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA308780 | ENA |
REPOSITORIES: ENA
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Project description:Maternal Plasma Folate impacts Differential DNA Methylation in an Epigenome-wide Meta-Analysis of Newborns
| PRJNA308779 | ENA
Project description:<p>Folic acid is routinely recommended for women trying to conceive to ensure proper fetal development. Mechanisms whereby periconceptional folate influences normal development and disease are poorly understood: epigenetics may be involved. This data represents meta-analysis results from a large epigenomics study to examine the association between maternal plasma folate during pregnancy and epigenome-wide DNA methylation using Illumina's HumanMethyl450 (450K) Beadchip in 1,996 newborns from two European cohorts. Results for all CpGs analyzed (419,905) are provided. </p> <p>These data may be downloaded through the dbGaP Authorized Access portal under phg000701.v1.</p>
| phs001059 | dbGaP
Project description:The mechanisms controlling genome methylation during human embryogenesis remain largely unknown. Here we provide evidence that maternal age at pregnancy permanently alters the epigenetic profile of offspring. We measured DNA methylation in blood at over 450,000 CpGs across the epigenome in 890 newborns.
2016-06-08 | GSE82273 | GEO
Project description:Pediatric acute lymphoblastic leukemia (ALL) is believed to originate in utero and frequently involves aberrant promoter methylation. Folate is the methyl donor for DNA methylation, suggesting that maternal folate metabolism may contribute to the development of ALL. We previously reported significant associations between single nucleotide polymorphisms (SNPs) in the maternal methionine synthase (MTR) gene and offspring’s risk of ALL. Here, we test the associations of 11 SNPs in MTR with aberrant DNA methylation in offspring with ALL. We recruited 51 ALL case-mother pairs from Texas Children’s Hospital from 2005-2010. We collected maternal saliva samples and diagnostic bone marrow plasma from cases. Bone marrow plasma was obtained from six healthy donors. DNA methylation was determined using MCA-Seq. Pyrosequencing was used to determine maternal MTR genotypes. We identified offspring with high and low promoter methylation and used logistic regression to estimate the effects of maternal genotype on offspring methylation. Twenty-two cases (43%) demonstrated high promoter methylation. Maternal MTR 113A>G was associated with aberrant DNA methylation in offspring (OR 4.59, 95% CI 1.21-17.93). To the best of our knowledge, this is the first report of an association between maternal genotype and offspring methylation in pediatric ALL.
2018-05-03 | GSE99793 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE36812: Epigenome analysis of cord blood samples from newborns GSE36828: Genome-wide analysis of gene expression levels in placenta and cord blood samples from newborns babies GSE36829: Epigenome analysis of placenta samples from newborns GSE36852: Epigenome analysis of newborn placenta and cord blood samples Refer to individual Series
2012-03-28 | E-GEOD-36831 | biostudies-arrayexpress
Project description:Early life exposures are critical in fetal programming and may influence function and health in later life. Adequate maternal folate consumption during pregnancy is essential for healthy fetal development and long-term offspring health. The mechanisms underlying fetal programming are poorly understood, but are likely to involve gene regulation. Epigenetic marks, including DNA methylation, regulate gene expression and are modifiable by folate supply. We observed before transcriptional changes in fetal liver in response to maternal folate depletion and hypothesised that these changes are due to altered gene promoter methylation. Female C57BL/6J mice were fed diets containing 2âmg or 0.4âmg folic acid/kg for 4âweeks before mating and throughout pregnancy. At 17.5 day gestation, genome-wide gene expression and promoter methylation were measured by microarray analysis in male fetal livers.
2016-06-14 | E-MTAB-4013 | biostudies-arrayexpress
Project description:Background: During gestation, stressors to the fetus, including viral exposure or maternal psychological distress, can fundamentally alter the neonatal epigenome, and may be associated with long-term impaired developmental outcomes. The impact of in utero exposure to the COVID-19 pandemic on the newborn epigenome has yet to be described. Methods: This study aimed to determine whether there are unique epigenetic signatures in newborns who experienced otherwise healthy pregnancies that occurred during the COVID-19 pandemic (Project RESCUE). The pre-pandemic control and pandemic cohorts (Project RESCUE) included in this study are part of a prospective observational and longitudinal cohort study that evaluates the impact of elevated prenatal maternal stress during the COVID-19 pandemic on early childhood neurodevelopment. Using buccal swabs collected at birth, differential DNA methylation analysis was performed using the Infinium MethylationEPIC arrays and linear regression analysis. Pathway analysis and gene ontology enrichment were performed on resultant gene lists. Results: Widespread differential methylation was found between neonates exposed in utero to the pandemic and pre-pandemic neonates. In contrast, there were no apparent epigenetic differences associated with maternal COVID-19 infection during pregnancy. Differential methylation was observed among genomic sites that underpin important neurological pathways that have been previously reported in the literature to be differentially methylated because of prenatal stress, such as NR3C1. Conclusions: The present study reveals that the onset and continuation of the COVID-19 pandemic has fundamentally altered the epigenomes of newborns born during this time, even in otherwise healthy pregnancies, which should be considered in current and future epigenetic studies and may act as a critical biomarker of stress.
2023-11-08 | GSE229463 | GEO
Project description:Background: Down syndrome (DS) is associated with a wide range of phenotypes. To address the hypothesis that the genome-wide perturbation of gene regulation in DS is modulated by epigenetic changes, we performed an epigenome-wide association study (EWAS) on neonatal bloodspots comparing 196 newborns with DS and 439 newborns without DS. Results: We identified 652 epigenome-wide significant CpGs (P<7.67x10-8) and 1,052 differentially methylated regions (DMRs) across the genome. Differential methylation at promoters/enhancers correlated with gene expression changes in DS versus non-DS fetal liver hematopoietic stem/progenitor cells (HSPC) (P<0.0001). Two of the top 3 DS-associated CpGs overlapped RUNX1, and were highly significantly hypermethylated in DS newborns (P<1.0x10-21). The top two DMRs overlapped promoters of RUNX1 and FLI1, both important regulators of megakaryopoiesis. FLI1 expression was markedly reduced in DS fetal liver HSCs (P<0.0001) and myeloid progenitors (P<0.0001). By contrast, RUNX1 expression was increased in DS fetal liver myeloid progenitors (P<0.0001), consistent with selective hypermethylation of the RUNX1 P2 promoter, which dominates in embryonic development, but sparing the P1 promoter that drives definitive hematopoiesis. Targeted sequencing of GATA1 revealed somatic, preleukemic mutations in 16.3% DS newborns, consistent with the high frequency of these mutations in DS newborns. Removal of DS newborns with GATA1 mutations had minimal impact on the EWAS results. Conclusions: DS has profound, genome-wide effects on DNA methylation in hematopoietic cells in early life, which may contribute to the high frequency of hematological problems, including leukemia, in children with DS. Blood-detectable DS-related epigenetic changes may underlie an array of DS outcomes, including neurologic and immune-related morbidities.
2020-12-04 | GSE160637 | GEO
Project description:Using HELP-Tagging, we defined the cytosine methylation profiles of hematopoietic stem/progenitor cells (CD34+) from umbilical cord blood in 29 healthy newborns. We found substantial variation of DNA methylation to occur in human CD34+ hematopoietic stem and progenitor cells from different individuals. Empirical annotation of the genome of this cell type reveals the variability to be targeted to candidate promoters and to candidate enhancer sequences of genes expressed at lower levels. The variability of DNA methylation at candidate enhancers was low for housekeeping genes but high for genes associated with leukocyte differentiation. The enrichment of DNA methylation variability at loci with intermediate methylation values, occurring at apparently “poised” enhancers, suggests cell subpopulation heterogeneity between individuals as the basis for the epigenomic variability observed. The “meta-epigenome” present even in purified cells complicates the design and interpretation of epigenome-wide association studies, but also allows insights into the gene expression characteristics and the number of cell types comprising the cell population analyzed. One Sentence Summary: Variability in epigenomic patterns between different individuals occurs predominantly at promoters and enhancers, reflecting cell subpopulation heterogeneity.
2014-07-01 | GSE49836 | GEO
Project description:These analyses set out to evaluate placental genomic and epigenomic signatures in newborns from the Extremely Low Gestational Age Newborns (ELGAN) cohort. Genome-wide mRNA, microRNA, and DNA methylation profiles were obtained from placenta samples collected at birth. Analyses were conducted to better understand placental molecular signatures and relate these to placental, maternal, infant, and later-in-life health indices.
2021-03-01 | GSE167885 | GEO