Ontology highlight
ABSTRACT:
PROVIDER: PRJNA740026 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14883051.fastq.gz | Fastqsanger.gz | |||
| SRR14883052.fastq.gz | Fastqsanger.gz | |||
| SRR14883053.fastq.gz | Fastqsanger.gz | |||
| SRR14883054.fastq.gz | Fastqsanger.gz | |||
| SRR14883055.fastq.gz | Fastqsanger.gz |
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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:Transgenerational effects of early experience on behavioural, hormonal and gene expression responses to acute stress in the precocial chicken. The data for the parental stressed and control birds is available in ArrayExpress with accession E-MTAB-924, while this experiment only concerns their offspring that never been exposed to early life stress.
2012-01-02 | E-MTAB-925 | biostudies-arrayexpress
Project description:Adverse experiences in early life are risk factors for the development of behavioral and physiological symptoms that can lead to psychiatric and cognitive disorders later in life. Some of these symptoms can be transmitted to the offspring, in some cases by non-genomic mechanisms involving germ cells. Using a mouse model of unpredictable maternal separation and maternal stress, we show that postnatal trauma alters coping behaviors in adverse conditions in exposed males when adult and in their adult male progeny. The behavioral changes are accompanied by increased glucocorticoid receptor (GR) expression and decreased DNA methylation of the GR promoter in the hippocampus. DNA methylation is also decreased in sperm cells of exposed males when adult. Transgenerational transmission of behavioral symptoms is prevented by paternal environmental enrichment, an effect associated with the reversal of alterations in GR gene expression and DNA methylation in the hippocampus of the male offspring. These findings highlight the influence of both, negative and positive environmental factors on behavior across generations, and the plasticity of the epigenome across life.
2018-10-26 | PXD004073 | Pride
Project description:Maternal exposure to social stress during pregnancy is associated with an increased risk of psychiatric disorders in the offspring in later life. How the effects of maternal social stress are transmitted to the developing foetus is unclear. Using a rat model of maternal social stress during pregnancy, we explored the mechanisms by which maternal stress is conveyed to the foetus and the potential for targeted treatment to prevent disease in the offspring. Maternal stress induced oxidative stress in the placenta, but not in the foetal brain, which was prevented by a single administration of nanoparticle-bound antioxidant prior to the stress exposure. Moreover, this antioxidant treatment prevented prenatal stress-induced anxiety-like behaviour in juvenile male offspring, along with neurological and gene expression changes in the offspring brain. In vitro, placental conditioned medium or foetal plasma from stressed pregnancies caused changes to cultured cortical neurons, similar to those observed in the brains of juvenile offspring exposed to prenatal stress, and were found to contain altered levels of extracellular microRNAs but not corticosterone. The present study highlights the crucial role of the placenta, and molecules secreted from the placenta, in foetal brain development and provides evidence of the potential for treatment that can prevent maternal stress-induced foetal programming of neurological disease.
2024-04-22 | GSE131040 | GEO
Project description:We show that traumatic stress experienced by males in early postnatal life impairs memory in their offspring, blocks long-term potentiation (LTP) and favors long-term depression (LTD). These effects are accompanied by suppression of key molecular pathways involved in neuronal plasticity both at rest and after acute stress. Male mice were exposed to chronic traumatic stress in early postnatal life and were later bred to naM-CM-/ve females to produce second-generation offspring. Memory performance was evaluated in the offspring, and synaptic plasticity was examined in the hippocampus and the amygdala, brain areas important for memory formation. The two groups tested were 1: offspring of fathers which were stressed (MSUS - maternal separation unpredictable stress) and 2: offspring of non-stressed fathers (control). Genome-wide gene expression in hippocampus of these two groups was assessed at rest and after acute stress (this study).
2014-07-01 | E-GEOD-47847 | biostudies-arrayexpress
Project description:We show that traumatic stress experienced by males in early postnatal life impairs memory in their offspring, blocks long-term potentiation (LTP) and favors long-term depression (LTD). These effects are accompanied by suppression of key molecular pathways involved in neuronal plasticity both at rest and after acute stress. Male mice were exposed to chronic traumatic stress in early postnatal life and were later bred to naM-CM-/ve females to produce second-generation offspring. Memory performance was evaluated in the offspring, and synaptic plasticity was examined in the hippocampus and the amygdala, brain areas important for memory formation. The two groups tested were 1: offspring of fathers which were stressed (MSUS - maternal separation unpredictable stress) and 2: offspring of non-stressed fathers (control). Genome-wide gene expression in hippocampus of these two groups was assessed at rest (this study) and after acute stress.
2014-07-01 | E-GEOD-47846 | biostudies-arrayexpress
Project description:Adverse early life experiences are well-established risk factors for neurological disorders later in life. However, the molecular mechanisms underlying the impact of adverse experiences on neurophysiological systems throughout life remain incompletely understood. Previous studies suggest that social attachment to parents in early development are indispensable for infants to grow into healthy adults. In situations where multiple offspring are born in a single birth in common marmosets, human hand-rearing is employed to ensure the survival of the offspring in captivity. However, hand-reared marmosets often exhibit behavioral abnormalities, including abnormal vocalizations, excessive attachment to the caretaker, and aggressive behavior. In this study, comprehensive transcriptome analyses were conducted on hippocampus tissues, a neuroanatomical region sensitive to social attachment, obtained from human hand-reared (N = 6) and parent-reared male marmosets (N = 5) at distinct developmental stages. Our analyses revealed consistent alterations in a subset of genes, including those related to neurodevelopmental diseases, across different developmental stages, indicating their continuous susceptibility to the effects of early parental deprivation. These findings highlight the dynamic nature of gene expression in response to early life experiences and suggest that the impact of early parental deprivation on gene expression may vary across different stages of development.
2024-01-04 | GSE236481 | GEO
Project description:There is extensive variation in DNA methylation between individuals and ethnic groups. These differences can arise from a combination of genetic and non-genetic influences and potential modifiers include nutritional cues, early life experience, and social and physical environments. Here we have assayed genome-wide DNA methylation in neonatal cord blood from African American, European American, and other ancestral groups. This is part of the CANDLE Study (Conditions Affecting Neurocognitive Development and Learning in Early Childhood). Our overarching goal is to determine the different environmental and maternal factors that can modify DNA methylation in newborns.
2015-01-14 | GSE64940 | GEO
Project description:Individual differences in basal leukocyte gene expression profiles as a function of hedonic and eudaimonic well-being, and psychological and social sub-dimensions of eudaimonic well-being. Gene expression profiling was carried out on peripheral blood mononuclear cell RNA samples collected from 122 healthy adults measured for hedonic and eudaimonic dimensions of well-being using the Short Flourishing Scale (Keyes, C (2014). The Mental Health Continuum-Short Form (MHC-SF) for adults). Higher values of the hedonic well-being scale indicate greater levels of positive affect, higher values of eudaimonic well-being scale indicate greater experience of purpose and meaning in life, higher values of social well-being scale indicate greater experience of social well-being in life, higher values of psychological well-being scale indicate greater experience of psychological well-being in life, greater TotalMHCSF scores indicate greater experience of all forms of well-being measured by the MHC-SF, the FlourishGroup indicates idividuals showing flourishing mental health as defined by the MHC-SF scoring instructions referenced above, greater BrownPsychological scores indicate greater experience of psychological well-being as measured by the MHC-SF with an alternative scoring, and greater BrownSocial scores indicate greater experience of social well-being as measured by the MHC-SF with an alternative scoring.
2015-03-28 | E-GEOD-55762 | biostudies-arrayexpress
Project description:Maternal exposure to stress during pregnancy is associated with an increased risk of psychiatric disorders in the offspring in later life. The mechanisms through which the effects of maternal stress are transmitted to the fetus are unclear, however the placenta, as the interface between mother and fetus, is likely to play a key role. Using a rat model, we investigated a role for placental oxidative stress in conveying the effects of maternal social stress to the fetus and the potential for treatment using a nanoparticle-bound antioxidant to prevent adverse outcomes in the offspring. Maternal psychosocial stress increased circulating corticosterone in the mother, but not in the fetuses. Maternal stress also induced oxidative stress in the placenta, but not in the fetal brain. Blocking oxidative stress using an antioxidant prevented the prenatal stress-induced anxiety phenotype in the male offspring, and prevented sex-specific neurobiological changes, specifically a reduction in dendrite lengths in the hippocampus, as well as reductions in the number of parvalbumin-positive neurons and GABA receptor subunits in the hippocampus and basolateral amygdala of the male offspring. Importantly, many of these effects were mimicked in neuronal cultures by application of placental-conditioned medium or fetal plasma from stressed pregnancies, indicating molecules released from the placenta may mediate the effects of prenatal stress on the fetal brain. Indeed, both placenta-conditioned medium and fetal plasma contained differentially abundant microRNAs following maternal stress, and their predicted targets were enriched for genes relevant to nervous system development and psychiatric disorders. The results highlight placental oxidative stress as a key mediator in transmitting the maternal social stress effects on the offspring's brain and behaviour, and offer a potential intervention to prevent stress-induced fetal programming of affective disorders.
2020-12-01 | GSE130573 | GEO