Metabolic Effects of Air Pollution Exposure and Reversibility
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PROVIDER: PRJNA608484 | ENA |
REPOSITORIES: ENA
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Project description:In this study, we modeled early life air pollution exposure using C57BL/6J male mice on a controlled chow diet, exposed to real-world inhaled concentrated PM2.5 (~10x ambient level/ ~60-120g/m3) or filtered air (FA) over 14 weeks. We investigated PM2.5 effects on phenotype, transcriptome and chromatin accessibility, compared the effects with a prototypical high-fat diet (HFD) stimulus, and examined the effects of cessation of exposure on reversibility of phenotype/genotype.
2020-11-05 | GSE145840 | GEO
Project description:Empirical evidence from both animals and humans suggest that PM2.5 (particulate matter < 2.5μm) exposure accelerates a variety of non-communicable diseases (NCDs) including Type 2 diabetes. We investigated whether chronic exposure to ambient air pollution (PM2.5), disrupts circadian rhythm to facilitate metabolic insulin resistance and compared the impact of inhaled ambient PM2.5 alone or in combination with continuous light exposure (LL). Exposure to PM2.5 induced peripheral IR, disrupted circadian steroid release, reduced peak oxygen consumption and altered brown adipose 18Ffluorodeoxyglucose uptake on PET imaging. These findings were identical to that seen with LL with no additive interaction between PM2.5 and LL. Transcriptome profiles in the liver revealed a number of differentially expressed circadian genes Bmal1 (Arntl/Npas2), Period (Per) and Cryptochrome (Cry) in response to PM2.5. Alteration in chromatin accessibility in circadian targets was observed with PM2.5 by Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq) while chromatin immunoprecipitation (ChIP) analysis, showed a marked difference in promoter occupancy by p300. Our data suggest a previously unrecognized role of particulate air pollution in promoting circadian disruption and metabolic dysfunction through epigenetic regulation of multiple circadian targets
2020-12-01 | GSE145566 | GEO
Project description:Effects of gestational exposure to air pollution on placental transcriptome
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Project description:Gestational exposure to air pollution increases the risk of autism spectrum disorder and cognitive impairments with unresolved molecular mechanisms. This study exposed mice throughout gestation to urban derived nanosized particulate matter (nPM). Young adult male and female offspring were studied for behavioral and metabolic changes using forced swim test, fat gain, glucose tolerance, and hippocampal transcriptome. Gestational nPM exposure caused increased depressive behaviors, decreased neurogenesis in the dentate gyrus, and increased glucose tolerance in adult male offspring. Both sexes gained fat and body weight. Gestational nPM exposure induced 29 differentially expressed genes (DEGs) in adult hippocampus related to cytokine production, IL17a signaling, and dopamine degradation in both sexes. Stratification by sex showed 2-fold more DEGs in males than females (69 vs 37), as well as male-specific enrichment of DEGs mediating serotonin signaling, endocytosis, Gai, and cAMP signaling. Gene co-expression analysis (WCGNA) identified a module of 43 genes with divergent responses to nPM between the sexes. Chronic changes in 14 DEGs (e.g., miR9-1) were associated with depressive behaviors, adiposity and glucose intolerance. These genes enriched neuroimmune pathways such as HMGB1 and TLR4. Based on cerebral cortex transcriptome data of neonates, we traced the initial nPM responses of HMGB1 pathway. In vitro, mixed glia responded to 24 h nPM with lower HMGB1 protein and increased proinflammatory cytokines. This response was ameliorated by TLR4 knockdown. In sum, we identified transcriptional changes that could underlie air pollution mediated behavioral and phenotypic changes. These identified genes merit further studies for therapeutic intervention development.
2020-07-07 | GSE147842 | GEO
Project description:The study comprises of 24 subjects that have been exposed to high and low Traffic-related air pollution.
2022-01-01 | GSE125647 | GEO
Project description:Air pollutants including particulate matter (PM) and chemicals adsorbed onto PM pose a serious threat to human health. In this study, we analyzed the ability of PM to induce diverse gene expression profile modulation after chronic exposure in subjects living in two regions of the Czech Republic differing in levels and sources of the air pollution. We also considered impact of different seasonal conditions on concentrations and compositions of PM. Blood samples of 312 subjects from polluted Ostrava city and 154 controls from Prague city were collected in winter 2009, summer 2009 and winter 2010. The highest concentrations of air pollutants were detected in winter 2010 when the subjects were exposed to: PM of aerodynamic diameter < 2.5 M-BM-5m (70 vs. 44.9 M-BM-5g/m3); benzo[a]pyrene (9.02 vs. 2.56 ng/m3) and benzene (10.2 vs. 5.5 M-BM-5g/m3) in Ostrava and Prague, respectively. Global gene expression analysis of total RNA extracted from leukocytes was performed using whole genome microarrays (Illumina). The expression of selected genes was verified by quantitative real-time PCR (qRT-PCR). Despite lower concentrations of air pollutants we found a higher number of differentially expressed genes and affected KEGG pathways in subjects from Prague. In both locations we observed differences between seasons. The qRT-PCR analysis showed a significant decrease in expression of APEX, ATM, FAS, GSTM1, IL1B and RAD21 in subjects from Ostrava, in a comparison of winter 2010 and summer 2009. In Prague, an increase in gene expression was observed for GADD45A and PTGS2. In conclusion, high concentrations of pollutants in Ostrava do not increase the number of differentially expressed genes. This may be explained by adaption of humans to chronic exposure to air pollution. Total RNA was extracted from leukocytes of total of 154 control subjects and 312 subjects exposed to heavy air pollution. The samples were collected in three seasons (winter 2009, summer 2009, winter 2010) with different levels of air pollution. Most of the subjects were sampled repeatedly; however, some of them joined the study in summer 2009 or winter 2010.
2014-08-27 | E-GEOD-60767 | biostudies-arrayexpress
Project description:We report the expression pattern of placental transcriptome by Next Generation Sequencing from Gestational D19 mouse exposed to Air -Pollutant material with or without prior treatment with Fish Oil.
2022-05-25 | GSE178098 | GEO
Project description:While environmental agents such as air pollution have been shown to be causative to diseases, yet limited knowledge exist on their mechanism of action. Here we used RNA-sequencing in combination with specific immunoprecipitation of 8-oxo-7,8-dihydroguanosine (8-oxoG) to identify transcripts accumulating oxidation after exposure to air pollution (derived from the reaction of 790 ppb acrolein, 670 ppb methacrolein, and 4 ppm ozone) in bronchial epithelial BEAS-2B cells. Results from this analysis suggest a functional role of the 8-oxoG modified transcripts after air pollution exposure in pathways that are central regulators of cell metabolism, growth, proliferation and maintenance of cellular structure. This study highlights a critical role for a RNA epitranscriptomics modification that can be used to further characterize biological responses to external stressors once considered indistinguishable.
2020-07-27 | GSE123933 | GEO
Project description:Comparison of genome-wide gene expression between humans living in areas of high levels of air pollution and less polluted areas. Keywords: Comparison of genome-wide gene expression between different conditions
2008-04-17 | GSE7543 | GEO
Project description:SINERGIA-Phyllosphere bacteria and air pollution
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