Epigenetic profiling changes of early adulthood with perinatal polychlorinated biphenyls and polychlorinated dibenzofurans exposure (Yucheng second generation) [methylation]
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PROVIDER: PRJNA492246 | ENA |
REPOSITORIES: ENA
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Project description:Genome-wide DNA methylation profiling of peripheral blood mononuclear cells from 30 male offspring from the Yucheng (perinatal polychlorinated biphenyls and polychlorinated dibenzofurans exposure) cohort and 30 male offspring from the Yucheng' neighborhood referents with similar backgrounds. The Infinium HumanMethylation450 BeadChip was used to obtain DNA methylation profiles across appromixmately 480,000 CpGs.
2018-09-21 | GSE120228 | GEO
Project description:Hornyhead turbot (Pleuronichthys verticalis), a sentinel flatfish species, were intraperitoneally injected with environmentally relevant mixtures of polybrominated diphenyl ethers (PBDEs) or polychlorinated biphenyls (PCBs). After 96 h, fish were sacrificed and liver tissue was collected for gene expression analysis using a custom-designed microarray.
2020-10-01 | GSE151532 | GEO
Project description:Biodegrades polychlorinated biphenyls
| PRJNA254 | ENA
Project description:Early life environmental exposure, particularly during perinatal period, can have a lifelong impact on organismal development and physiology. The biological rationale for this phenomenon is to promote physiological adaptation to the anticipated environment based on early life experience. However, perinatal exposure to adverse environments can also be associated with adult-onset disorders. Multiple environmental stressors induce glucocorticoids, which prompted us to investigate their role in developmental programming. Here, we report that perinatal glucocorticoid exposure had long-term consequences and resulted in diminished CD8 T cell response in adulthood and impaired control of tumor growth and bacterial infection. We found that perinatal glucocorticoid exposure resulted in persistent alteration of the hypothalamic-pituitaryadrenal (HPA) axis. Consequently, the level of the hormone in adults was significantly reduced, resulting in decreased CD8 T cell function. Our study thus demonstrates that perinatal stress can have long-term consequences on CD8 T cell immunity by altering HPA axis activity.
2020-01-01 | GSE136978 | GEO
Project description:Early life environmental exposure, particularly during perinatal period, can have a lifelong impact on organismal development and physiology. The biological rationale for this phenomenon is to promote physiological adaptation to the anticipated environment based on early life experience. However, perinatal exposure to adverse environments can also be associated with adult-onset disorders. Multiple environmental stressors induce glucocorticoids, which prompted us to investigate their role in developmental programming. Here, we report that perinatal glucocorticoid exposure had long-term consequences and resulted in diminished CD8 T cell response in adulthood and impaired control of tumor growth and bacterial infection. We found that perinatal glucocorticoid exposure resulted in persistent alteration of the hypothalamic-pituitaryadrenal (HPA) axis. Consequently, the level of the hormone in adults was significantly reduced, resulting in decreased CD8 T cell function. Our study thus demonstrates that perinatal stress can have long-term consequences on CD8 T cell immunity by altering HPA axis activity.
2020-01-01 | GSE136972 | GEO
Project description:11 Arctic fox samples were analyzed to see if blood cells contained polychlorinated biphenyls (PCBs) and/or mercury.
2017-07-18 | GSE71407 | GEO
Project description:We analyzed the transcriptional response of the actinomycete Rhodococcus aetherivorans I24 to biphenyl and polychlorinated biphenyls (PCBs). This species has not been extensively exposed to PCBs, as it was first isolated from a toluene contaminated aquifer, rather than a site contaminated with polychlorinated hydrocarbons. Using a microarray targeting 3524 genes, we assessed gene expression in minimal medium supplemented with various substrates (e.g. PCBs) and in both PCB-contaminated and non-contaminated sediment slurries. Relative to the reference condition (minimal medium supplemented with glucose), 408 genes were up-regulated in the various treatments. In medium and in sediment, PCBs elicited the up-regulation of a common set of 100 genes, including chaperones (groEL), a superoxide dismutase (sodA), alkyl hydroperoxide reductase protein C (ahpC), and a catalase/peroxidase (katG). Analysis of the R. aetherivorans I24 genome sequence identified orthologs of many of the genes in the canonical biphenyl pathway, but very few of these genes were up-regulated in response to PCBs or biphenyl. This study is one of the first which utilizes microarrays to assess the transcriptional response of a soil bacterium to a pollutant under conditions which more closely resemble the natural environment. Our results indicate that the transcriptional response of R. aetherivorans I24 to PCBs, in both medium and sediment, is primarily directed towards reducing oxidative stress, rather than catabolism. In addition, the identification of numerous genes expressed in contaminated soil specifically may have implications for the development of biosensors. Finally, comparative genomic and transcriptomic analyses suggest that the mere presence of orthologs of the required enzymes may not be sufficient to confer a vigorous biphenyl/PCB metabolism. RNA was isolated from cells incubated in the following: sediment from a PCB-contaminated industrial site, uncontaminated sediment from a comparable site, and defined media supplemented with glucose (3 g/L), glucose and biphenyl (3 g/L, 4.5 μM), or glucose and PCBs (3 g/L, 5 mg/L Aroclor 1254). In all cases, there were 3 biological replicates and 2 technical replicates (repeat hybridizations). A total of 3524 genes are represented on the arrays; of these, 41 and 176 are found on the plasmids pRA2 and pRA3, respectively. On average, there are 3 distinct 24nt probes per gene.
2010-03-20 | E-GEOD-17033 | biostudies-arrayexpress
Project description:We analyzed the transcriptional response of the actinomycete Rhodococcus aetherivorans I24 to biphenyl and polychlorinated biphenyls (PCBs). This species has not been extensively exposed to PCBs, as it was first isolated from a toluene contaminated aquifer, rather than a site contaminated with polychlorinated hydrocarbons. Using a microarray targeting 3524 genes, we assessed gene expression in minimal medium supplemented with various substrates (e.g. PCBs) and in both PCB-contaminated and non-contaminated sediment slurries. Relative to the reference condition (minimal medium supplemented with glucose), 408 genes were up-regulated in the various treatments. In medium and in sediment, PCBs elicited the up-regulation of a common set of 100 genes, including chaperones (groEL), a superoxide dismutase (sodA), alkyl hydroperoxide reductase protein C (ahpC), and a catalase/peroxidase (katG). Analysis of the R. aetherivorans I24 genome sequence identified orthologs of many of the genes in the canonical biphenyl pathway, but very few of these genes were up-regulated in response to PCBs or biphenyl. This study is one of the first which utilizes microarrays to assess the transcriptional response of a soil bacterium to a pollutant under conditions which more closely resemble the natural environment. Our results indicate that the transcriptional response of R. aetherivorans I24 to PCBs, in both medium and sediment, is primarily directed towards reducing oxidative stress, rather than catabolism. In addition, the identification of numerous genes expressed in contaminated soil specifically may have implications for the development of biosensors. Finally, comparative genomic and transcriptomic analyses suggest that the mere presence of orthologs of the required enzymes may not be sufficient to confer a vigorous biphenyl/PCB metabolism.
2010-03-20 | GSE17033 | GEO
Project description:Selective serotonin reuptake inhibitor (SSRI) antidepressants are the mainstay treatment for the 10-20% of pregnant and postpartum women who suffer major depression, but the effects of SSRIs on their children’s developing brain and later emotional health are poorly understood. SSRI use during pregnancy can elicit antidepressant withdrawal in newborns and increase toddlers’ anxiety and social avoidance. In rodents, perinatal SSRI exposure increases adult depression- and anxiety-like behavior, although certain individuals are more vulnerable to these effects than others. Our study establishes a rodent model of individual differences in susceptibility to perinatal SSRI exposure, utilizing selectively-bred Low Responder (LR) and High Responder (HR) rats that were previously bred for high versus low behavioral response to novelty. Pregnant HR/LR females were chronically treated with the SSRI paroxetine (10 mg/kg/day p.o.) to examine its effects on offspring’s emotional behavior and gene expression in the developing brain. Paroxetine treatment had minimal effect on HR/LR dams’ pregnancy outcomes or maternal behavior. We found that LR offspring, naturally prone to an inhibited/anxious temperament, were susceptible to behavioral abnormalities associated with perinatal SSRI exposure (which exacerbated their Forced Swim Test immobility), while high risk-taking HR offspring were resistant. Microarray studies revealed robust perinatal SSRI-induced gene expression changes in the developing LR hippocampus and amygdala (postnatal days 7-21), including transcripts involved in neurogenesis, synaptic vesicle components, and energy metabolism. These results highlight the LR/HR model as a useful tool to explore the neurobiology of individual differences in susceptibility to perinatal SSRI exposure.
2018-03-03 | GSE111362 | GEO
Project description:Background: It is postulated that the developmental defects frequently observed in somatic clones arise from inappropriate reprogramming of the donor epigenome by the oocyte. We used cattle clones as a model to investigate the long-term effects of nuclear reprogramming on both DNA methylation and the phenotype of a differentiated organ, the liver. Pathological perinatal clones and apparently normal adult clones, both produced within one decade, were studied, together with age-matched controls. Results: Using MeDIP-chip, we identified differentially methylated regions (DMRs) in gene promoters displaying variations according to age and to the clone status of the animals. Strikingly, whereas adult clones did not differ significantly from adult controls, perinatal clones showed a demethylation at DMRs inconsistent with their chronological age. Pathological features were found in the liver of perinatal clones only, with histological lesions and modifications to both histomorphometrical and metabolic parameters. The integration of DMRs with phenotypic datasets led to the identification of epigenetic alterations correlated to phenotypic abnormalities in perinatal clones. Genes important to the antioxidant response and energy metabolism were targeted by these alterations. For at least one DMR, the aberrant methylation profile in perinatal clones was associated with altered gene expression. Conclusions: The liver defects encountered in pathological perinatal clones could be associated to the aberrant age of DNA methylation, at genes indicating potential deficits in oxidative metabolism. We propose that epigenetic ageing is an adaptation to the excessive oxidative stress induced by reprogramming that the pathological clones were not able to counteract during subsequent developmental stages.
2016-12-21 | GSE73028 | GEO