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Cerebral cortex and blood transcriptome changes in mouse neonates prenatally exposed to air pollution particulate matter

ABSTRACT: Cerebral cortex and blood transcriptome changes in mouse neonates prenatally exposed to air pollution particulate matter

PROVIDER: PRJNA597046 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10748858_1.fastq.gz	Fastqsanger.gz
	SRR10748858_2.fastq.gz	Fastqsanger.gz
	SRR10748859_1.fastq.gz	Fastqsanger.gz
	SRR10748859_2.fastq.gz	Fastqsanger.gz
	SRR10748860_1.fastq.gz	Fastqsanger.gz

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Cerebral cortex and blood transcriptome changes in mouse neonates prenatally exposed to air pollution particulate matter

Project description:Background: Prenatal exposure to air pollutants is associated with increased risk for neurodevelopmental and neurodegenerative disorders. However, few studies have identified transcriptional changes related to air pollutant exposure. Methods: RNA sequencing was used to examine transcriptomic changes in blood and cerebral cortex of three male and three female mouse neonates prenatally exposed to traffic-related nano-sized particulate matter (nPM) compared to three male and three female mouse neonates prenatally exposed to control filter air. Results: We identified 19 nPM-associated differentially expressed genes (nPM-DEGs) in blood and 124 nPM-DEGs in cerebral cortex. The cerebral cortex transcriptional responses to nPM suggested neuroinflammation involvement, including CREB1, BDNF, and IFN γ genes. Both blood and brain tissues showed nPM transcriptional changes related to DNA damage, oxidative stress, and immune responses. Three blood nPM-DEGs showed a canonical correlation of 0.98 with 14 nPM-DEGS in the cerebral cortex, suggesting a convergence of gene expression changes in blood and cerebral cortex. Exploratory sex-stratified analyses suggested a higher number of nPM-DEGs in female cerebral cortex than male cerebral cortex. The sex-stratified analyses identified 2 nPM-DEGs (Rgl2 and Gm37534) shared between blood and cerebral cortex in a sex-dependent manner. Conclusions: Our findings suggest that prenatal nPM exposure induces transcriptional changes in the cerebral cortex, some of which are also observed in blood. Further research is needed to replicate nPM-induced transcriptional changes with additional biologically relevant time points for brain development.

2021-08-25 | GSE142453 | GEO

Cerebral cortex and blood transcriptome changes in mouse neonates prenatally exposed to air pollution particulate matter.

Project description:BackgroundPrenatal exposure to air pollutants is associated with increased risk for neurodevelopmental and neurodegenerative disorders. However, few studies have identified transcriptional changes related to air pollutant exposure.MethodsRNA sequencing was used to examine transcriptomic changes in blood and cerebral cortex of three male and three female mouse neonates prenatally exposed to traffic-related nano-sized particulate matter (nPM) compared to three male and three female mouse neonates prenatally exposed to control filter air.ResultsWe identified 19 nPM-associated differentially expressed genes (nPM-DEGs) in blood and 124 nPM-DEGs in cerebral cortex. The cerebral cortex transcriptional responses to nPM suggested neuroinflammation involvement, including CREB1, BDNF, and IFNγ genes. Both blood and brain tissues showed nPM transcriptional changes related to DNA damage, oxidative stress, and immune responses. Three blood nPM-DEGs showed a canonical correlation of 0.98 with 14 nPM-DEGS in the cerebral cortex, suggesting a convergence of gene expression changes in blood and cerebral cortex. Exploratory sex-stratified analyses suggested a higher number of nPM-DEGs in female cerebral cortex than male cerebral cortex. The sex-stratified analyses identified 2 nPM-DEGs (Rgl2 and Gm37534) shared between blood and cerebral cortex in a sex-dependent manner.ConclusionsOur findings suggest that prenatal nPM exposure induces transcriptional changes in the cerebral cortex, some of which are also observed in blood. Further research is needed to replicate nPM-induced transcriptional changes with additional biologically relevant time points for brain development.

| S-EPMC8383458 | biostudies-literature

Exposure to particulate air pollution disrupts erythrocyte turnover

Project description:Exposure to particulate air pollution disrupts erythrocyte turnover

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Exposure to particulate air pollution disrupts erythrocyte turnover

Project description:Chronic exposure to ambient particulate matter (PM) increases the risk of cardiovascular disease (CVD). One proposed mechanism linking PM exposure and CVD is the induction of low-grade systemic inflammation that underlies disease progression. However, the intermediaries that relay signals from the proximal sites of inflammation to the periphery remain unknown. We have previously shown that fine PM (PM2.5) alter red blood cell distribution width. Therefore, the overall goal of this study was to elucidate how PM exposure impacts the spleen and splenic macrophages which are primarily responsible for the turnover of aged and damaged red blood cells.

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Project description:This study aimed to shed light on the gene regulatory networks underlying plant leaf responses to air particulate matter. Our investigation focused on shrubs of Photinia x fraseri grown in pots located in two contrasting areas: a highly polluted traffic road and rural countryside within the same town (Altopascio, Lucca, Italy). RNA-seq data were related to leaf morphological traitsand air particulate matter, allowing to identify key players in modulating the capabilities of plants to phyllo-remediate high air particulate matter levels in urban environment.

2023-03-23 | E-MTAB-12477 | biostudies-arrayexpress

Exposure to Air pollution Disrupts Circadian Rhythm through Alterations in Chromatin Dynamics

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

Gene expression analysis of breast adenocarninoma cell line T47D treated with particulate matter PM2.5 sampled near the municipal solid waste incineration plant of Bologna city.

Project description:We reported the gene expression profile of T47D cells treated with the organic extract of Particulate matter 2.5 (PM2.5) sampled next to the municipal solid waste incineration plant of Bologna city. Based on a air pollution distribution model that takes the incinaration plant as point source of emission, two sites were chosen to sample particulate matter near incineration plant: "FrulloEst" representing the maximum effect of the incineration plant, "Calamosco" representing the negative control of "FrulloEst" (minimun effect of incineration plant, same effect of other air pollution fonts). Another site, "Giardini Margherita", is chosen to sample the urban background air pollution. for each site sample collection was performed in winter and in summer season.

2018-01-31 | E-MEXP-3686 | biostudies-arrayexpress

Gene Expression Network Analyses in Response to Air Pollution Exposures in the Trucking Industry

Project description:To investigate the cellular responses induced by air pollution exposures, we performed genome-wide gene expression microarray analysis using whole blood RNA sampled at three time-points across the work weeks of 63 non-smoking employees in the trucking industry. Our objective was to identify the genes and gene networks differentially activated in response to micro-environmental measures of occupational exposure to three pollutants: PM2.5 (particulate matter ≤ 2.5 microns in diameter) and elemental carbon (EC) and organic carbon (OC).

2016-07-08 | GSE83864 | GEO

Developmental exposure to air pollution particulates increases asthma severity, alters the RNA transcriptome, and DNA methylation in female adult progeny [WGMS]

Project description:Maternal exposure to particulate air pollution increases the incidence and severity of asthma in offspring, yet the mechanisms for this are unclear. Known susceptibility loci are a minor component of this effect. We interrogate a mouse allergic airway disease model to assess epigenetic associations between maternal air pollution exposure and asthma-like responses in offspring. Maternal air pollution exposure increased allergic airway disease severity in adult offspring associated with a suppressed transcriptomic response to allergen. Control progeny showed differential expression of 2842 genes across several important pathways, including the SMAD and TGFβR pathways, whilst air pollutant progeny showed an 80% reduction in differentially expressed genes and abrogation of many pathway associations. Whole genome CpG methylome analysis following allergen challenge detected differential methylation regions across the genome. Approximately 20% of differentially expressed genes were associated with differential methylation. Differentially methylated regions were markedly reduced in offspring of air pollution exposed mothers, and this was most evident in intronic regions and some transposable element classes. This study shows that allergic airways disease in adult offspring of PM2.5 exposed mothers had a markedly repressed transcriptomic response, a proportion of which was associated with identifiable changes in the lung’s methylome. The results point to an epigenetic contribution to the severity of asthma in offspring of mothers exposed to particulate air pollution.

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suspended particulate matter

Project description:suspended particulate matter Raw sequence reads

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