Expression data on APM effect in vitro
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE18593 | GEO | 2011/12/02
SECONDARY ACCESSION(S): PRJNA121333
REPOSITORIES: GEO
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Project description:To seek whether seasonal variation in environmental particulate matter composition affected the global gene response patterns in cultured human cells representing pulmonary and systemic vascular targets. We used microarrays to detail the global program of gene expression affected on different cells type by different seasonal collections of Ambient Particulate Matter. After treatment with 10 ug/mL either summer2006 or winter2007APM, endothelial or bronchail epithelial cells were isolated by RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain the genes responses correlated with current concepts of systemic inflammation in cardiovascular effects of particulate air pollution.
2011-12-02 | E-GEOD-18593 | biostudies-arrayexpress
Project description:The aim of the present study was to characterize a common and unique signalling pathways associated to two seasonal particulate matter (PM) (winter PM2.5 and summer PM10) in human bronchial BEAS-2B cells by mean of a global transcriptomic profiling (including genes and miRNA) and the investigation of selected pathways at protein level.
2016-05-26 | E-MTAB-3629 | biostudies-arrayexpress
Project description:The aim of the present study was to characterize a common and unique signalling pathways associated to two seasonal particulate matter (PM) (winter PM2.5 and summer PM10) in human bronchial BEAS-2B cells by mean of a global transcriptomic profiling (including genes and miRNA) and the investigation of selected pathways at protein level.
2016-05-26 | E-MTAB-3630 | biostudies-arrayexpress
Project description:The purpose of this study was to characterize global gene expression in human airway epithelial cells and identify cellular pathways associated with coarse, fine and ultrafine particulate matter (PM) exposures. Ambient PM was collected in 3 different size fractions from Chapel Hill air, particles were extracted from foam or filter matrices and lyophilized. Human primary airway epithelial cells were exposed to particles at 250μg/ml or vehicle control for 6h in culture. Following exposure, RNA was isolated and hybridized to human HG U133A affymetrix chips. Keywords: particle treatment
2008-05-01 | GSE7010 | GEO
Project description:Murine Pulmonary Responses to Ambient Baltimore Particulate Matter
| PRJNA103235 | ENA
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
Project description:The purpose of this study was to characterize global gene expression in human airway epithelial cells and identify cellular pathways associated with coarse, fine and ultrafine particulate matter (PM) exposures. Ambient PM was collected in 3 different size fractions from Chapel Hill air, particles were extracted from foam or filter matrices and lyophilized. Human primary airway epithelial cells were exposed to particles at 250μg/ml or vehicle control for 6h in culture. Following exposure, RNA was isolated and hybridized to human HG U133A affymetrix chips. Experiment Overall Design: Human primary epithelial cells were exposed to coarse, fine, ultrafine PM or vehicle control in culture for 6h. Three biological replicates for each treatment (coarse, fine, ultrafine, control) were conducted at (250ug/ml). 12 Affymetrix chips (HG U133A) were used.
2008-06-15 | E-GEOD-7010 | biostudies-arrayexpress
Project description:Purpose: Determine the mechanism of particulate matter-induced signaling in melanocytes. Method: Primary human epidermal melanocytes were treated with particulate matter (5 μg/cm2) and incubated for 24 h. Total RNA (1 ug) from melanocytes were extracted and subjected to library synthesis. Results: Particulate matter-treated melanocytes exhibited upregulation of ER stress, unfolded protein response, and melanogenesis-related molecules. Conclusion: Particulate matter-induced melanocyte signaling was well evaluated using RNA sequencing.
2021-08-19 | GSE165333 | GEO
Project description:Particulate Matter Triggers Carotid Body Dysfunction, Respiratory Dysynchrony and Cardiac Arrhythmias in Mice with Cardiac Failure; The mechanistic link between human exposure to airborne particulate matter (PM) pollution and the increased cardiovascular morbidity and mortality observed in people with congestive heart failure (CHF) is unknown. We now show that exposure of genetically-engineered mice with CHF (expressing a cardiac-specific CREB mutant transcription factor) to ambient PM (collected in Baltimore, mean aerodynamic diameter 1.9 um) unmasks severe autonomic morbidities manifested as significant reductions in heart rate variability, respiratory dysynchrony and increased frequency of serious ventricular arrhythmias, features not observed in PM-challenged wild type mice without CHF. PM exposure in CREB mice with CHF reflexly triggers autonomic dysfunction via heightened carotid body function as evidenced by pronounced afferent nerve responses to hypoxia and marked depression of breathing by hyperoxia challenge. Genomic analyses of lung and ventricular tissues revealed PM-induced molecular signatures of inflammation and oxidative stress. These findings in a murine model of cardiac failure provide the first direct assessment of autonomic function in response to PM challenge and are highly consistent with current epidemiologic findings on cardiovascular morbidity in susceptible PM-exposed human populations. We utilized a murine model of dilated cardiomyopathy to address potential mechanistic links between PM exposure and the development of life-threatening cardiac dysrhythmias. Experiment Overall Design: four group (n=3) of animals were treated by PBS or particulate matter (20mg/kg 1.9µm particulate matter) in Wild type or CD-1 dominate negative mice
2009-08-15 | E-GEOD-17478 | biostudies-arrayexpress
Project description:Murine Pulmonary Responses to Ambient Baltimore Particulate Matter: Genomic Analysis and Contribution to Airway Hyperresponsiveness; Asthma is a complex disease characterized by airway hyperresponsiveness (AHR) and chronic airway inflammation. Environmental factors such as ambient particulate matter (PM), a major air pollutant, has been demonstrated in epidemiological studies to contribute to asthma exacerbation and increased asthma prevalence. OBJECTIVE: We investigated the genomic and pathophysiological effects of Baltimore PM (median diameter 1.78 µm) in a murine model of asthma to identify potential biomarkers. METHODS: A/J mice with ovalbumin (OVA) âinduced AHR were exposed to PM (20 mg/kg, intratracheal), and both AHR and bronchoalveolar lavage (BAL) were assayed on days 1, 4, and 7 post exposure. Lung gene expression profiling (Affymetrix Mouse430_ 2.0) by PM (20 mg/kg, intratracheal) were assayed on OVA- and / or PM--challenged mice. RESULTS: Significant increases of airway responsiveness in OVA-treated mice were observed, indicating an asthmatic phenotype. Ambient PM exposure induced significant changes in AHR in both naive mice and OVA-induced asthmatic mice. In both naive and OVA challenged asthmatic mice, PM induced eosinophil and neutrophil infiltration into airways, elevated BAL protein content, and stimulated secretion of TH1 cytokines (IFN-g, IL-6, and TNF-a) and TH2 cytokines (IL-4, IL-5, and eotaxin) into BAL. Consistent with these results, PM induced expression of genes of innate immune response, chemotaxis and complementary system. CONCLUSION: These studies, consistent with epidemiological data, indicate that PM increases AHR and lung inflammation in naïve mice and exacerbates the asthma phenotype of increased AHR and gene expression pattern changes correlated with acute lung inflammation and airway damage. We used microarrays to detail the global programme of gene expression induced by rhPBEF treatment and VALI. Experiment Overall Design: animals were treated by PBS, Oval albumin, PM, or both OVA/PM
2008-06-16 | E-GEOD-9465 | biostudies-arrayexpress