Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA373888 | ENA |
REPOSITORIES: ENA
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Project description:Early life social experiences are believed to confer persistent effects on individual’s biology and subsequent functioning and health. Using a diverse, longitudinal community sample of 178 children, we show that three different types of early life social experience: family income, parental education, and family psychosocial adversity, each predict DNA methylation within buccal epithelial cells. Each predictor was significantly associated with DNA methylation within a unique set of genomic CpG sites, with income showing the greatest number of associations. Findings were independently verified using pyrosequencing. Our results provide evidence for longitudinal associations between early life social environment and variation in DNA methylation during childhood, after adjusting for genetic ancestry and self-reported ethnic minority status. Gene ontology analyses of top, differentially methylated CpG sites point to genes serving immune and developmental regulation functions, suggesting potential pathways for the biological embedding of early life stress and its association with later development and health.
2018-12-07 | GSE94734 | GEO
Project description:Epigenetics is emerging as an attractive mechanism to explain the persistent genomic embedding of early-life experiences. Tightly linked to chromatin, which packages DNA into chromosomes, epigenetic marks primarily serve to regulate the activity of genes. DNA methylation is the most accessible and characterized component of the many chromatin marks that constitute the epigenome, making it an ideal target for epigenetic studies in human populations. Here, using peripheral blood mononuclear cells collected from a community-based cohort stratified for early-life socioeconomic status, we measured DNA methylation in the promoter regions of more than 14,000 human genes. Using this approach, we broadly assessed and characterized epigenetic variation, identified some of the factors that sculpt the epigenome, and determined its functional relation to gene expression.We found that the leukocyte composition of peripheral blood covaried with patterns of DNA methylation at many sites, as did demographic factors, such as sex, age, and ethnicity. Furthermore, psychosocial factors, such as perceived stress, and cortisol output were associated with DNA methylation, as was early-life socioeconomic status. Interestingly, we determined that DNA methylation was strongly correlated to the ex vivo inflammatory response of peripheral blood mononuclear cells to stimulation with microbial products that engage Toll-like receptors. In contrast, our work found limited effects of DNA methylation marks on the expression of associated genes across individuals, suggesting a more complex relationship than anticipated This cohort consist of genomic DNA extracted from 94 PBMC DNA samples, bisulphite converted and hybridized, along with 5 technical replicates to the Illumina Infinium HumanMethylation27 Beadchip v1.2 for genome wide DNA methylation profiling.
2012-10-10 | E-GEOD-37008 | biostudies-arrayexpress
Project description:Fifteen-year-old adolescents (N = 109) in a longitudinal study of child development were recruited to examine differences in DNA methylation in relation to parent reports of adversity during the adolescents’ infancy and preschool periods. Microarray technology applied to 28,000 cytosine–guanine dinucleotide sites within DNA derived from buccal epithelial cells showed differential methylation among adolescents whose parents reported high levels of stress during their children’s early lives. Maternal stressors in infancy and paternal stressors in the preschool years were most strongly predictive of differential methylation, and the patterning of such epigenetic marks varied by children’s gender. To the authors’ knowledge, this is the first report of prospective associations between adversities in early childhood and the epigenetic conformation of adolescents’ genomic DNA. Genomic DNA was extracted from 109 Buccal DNA samples, bisulphite converted and hybridized, along with 4 technical replicates to the Illumina Infinium HumanMethylation27 Beadchip v1.2 for genome wide DNA methylation profiling. Processed signal intensity data and Detection Pvalues for individual replicates of Samples 006 (reps a,b), 099 (reps a,b,c), 106 (reps a,b) reported in the supplementary file "processed_individual reps.txt."
2011-05-30 | E-GEOD-25892 | biostudies-arrayexpress
Project description:Epigenetics is emerging as an attractive mechanism to explain the persistent genomic embedding of early-life experiences. Tightly linked to chromatin, which packages DNA into chromosomes, epigenetic marks primarily serve to regulate the activity of genes. DNA methylation is the most accessible and characterized component of the many chromatin marks that constitute the epigenome, making it an ideal target for epigenetic studies in human populations. Here, using peripheral blood mononuclear cells collected from a community-based cohort stratified for early-life socioeconomic status, we measured DNA methylation in the promoter regions of more than 14,000 human genes. Using this approach, we broadly assessed and characterized epigenetic variation, identified some of the factors that sculpt the epigenome, and determined its functional relation to gene expression.We found that the leukocyte composition of peripheral blood covaried with patterns of DNA methylation at many sites, as did demographic factors, such as sex, age, and ethnicity. Furthermore, psychosocial factors, such as perceived stress, and cortisol output were associated with DNA methylation, as was early-life socioeconomic status. Interestingly, we determined that DNA methylation was strongly correlated to the ex vivo inflammatory response of peripheral blood mononuclear cells to stimulation with microbial products that engage Toll-like receptors. In contrast, our work found limited effects of DNA methylation marks on the expression of associated genes across individuals, suggesting a more complex relationship than anticipated
2012-10-10 | GSE37008 | GEO
Project description:Fifteen-year-old adolescents (N = 109) in a longitudinal study of child development were recruited to examine differences in DNA methylation in relation to parent reports of adversity during the adolescents’ infancy and preschool periods. Microarray technology applied to 28,000 cytosine–guanine dinucleotide sites within DNA derived from buccal epithelial cells showed differential methylation among adolescents whose parents reported high levels of stress during their children’s early lives. Maternal stressors in infancy and paternal stressors in the preschool years were most strongly predictive of differential methylation, and the patterning of such epigenetic marks varied by children’s gender. To the authors’ knowledge, this is the first report of prospective associations between adversities in early childhood and the epigenetic conformation of adolescents’ genomic DNA.
2011-05-30 | GSE25892 | GEO
Project description:Research shows that children who are reared in households with low socioeconomic status are more vulnerable to heart disease, respiratory infection, and some cancers when they reach adulthood. This study conducted transcriptional profiling of PBMC in healthy adults who were low vs. high in early-life SES to explore the long-lasting genomic effects of early experience. Keywords: life stress, gene expression, inflammation, socioeconomic status Samples from 30 adults with low early-life SES and 30 adults with high early-life SES
2009-03-10 | E-GEOD-15180 | biostudies-arrayexpress
Project description:Given the salient role of early-life adversity (ELA) and the resulting biological embedding in disease risk, there is a critical need to understand the mechanisms operating at multiple levels of analysis in order to promote effective clinical treatments and intervention efforts for survivors. An example for such an effort could be to utilize models of dynamic cellular markers as individual-level factors to account for variation in intervention response and clinical outcomes. Results of this study will lead to new knowledge about specific gene expression pathways in response to stress, and whether the response is moderated by previous exposure to early adversity, shorter telomere length (a marker of cellular aging) and self-report mental-health measures. Thus, the long-term effects of this study will advance our understanding on stress-related transcriptomic changes that play a downstream role in disease susceptibility and accelerated aging, with the goal of targeting specific pathways and genes for potential intervention studies and pharmacological treatments to reverse the effects of exposure to early adversity. For example, considering high failure rates for depression treatments, and in order to tailor individual interventions, identifying objective changes in stress-induced gene expression may help to predict intervention efficacy in clinical and non-clinical settings, as seen, for example, in breast and leukemia cancers. Thus, findings will have a range of impacts for basic science, intervention studies and clinical practice that will influence treatments to match the specific cellular processes operating within an individual.
2023-03-21 | GSE227812 | GEO
Project description:Given the salient role of early-life adversity and the resulting biological embedding in disease risk, there is a critical need to understand the mechanisms operating at multiple levels of analysis in order to promote effective clinical treatments and intervention efforts for survivors. An example for such an effort could be to utilize models of dynamic cellular markers as individual-level factors to account for variation in intervention response and clinical outcomes. Results of this study will lead to new knowledge about specific gene expression pathways in response to stress, and whether the response is moderated by previous exposure to early adversity, shorter telomere length (a marker of cellular aging) and self-report mental-health measures. Thus, the long-term effects of this study will advance our understanding on stress-related transcriptomic changes that play a downstream role in disease susceptibility and accelerated aging, with the goal of targeting specific pathways and genes for potential intervention studies and pharmacological treatments to reverse the effects of exposure to early adversity. For example, considering high failure rates for depression treatments, and in order to tailor individual interventions, identifying objective changes in stress-induced gene expression may help to predict intervention efficacy in clinical and non-clinical settings, as seen, for example, in breast and leukemia cancers. Thus, findings will have a range of impacts for basic science, intervention studies and clinical practice that will influence treatments to match the specific cellular processes operating within an individual.
2023-03-21 | GSE227809 | GEO
Project description:Research shows that children who are reared in households with low socioeconomic status are more vulnerable to heart disease, respiratory infection, and some cancers when they reach adulthood. This study conducted transcriptional profiling of PBMC in healthy adults who were low vs. high in early-life SES to explore the long-lasting genomic effects of early experience. Keywords: life stress, gene expression, inflammation, socioeconomic status
2009-03-11 | GSE15180 | GEO
Project description:DNA Methylation Differences Associated with Social Anxiety Disorder and Early Life Adversity
| PRJNA688716 | ENA