E-MTAB-2751
Ontology highlight
ABSTRACT:
TISSUE(S): Heart, Lung
PROVIDER: E-MTAB-2751 | ExpressionAtlas | 2015-07-13
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-2751-analysis-methods.tsv | Tabular | |||
| E-MTAB-2751-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-2751-configuration.xml | Xml | |||
| E-MTAB-2751-percentile-ranks.tsv | Tabular | |||
| E-MTAB-2751.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 53 |
Similar Datasets
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:We examined the impact of chronic lung inflammation on the pulmonary transcriptional response to inhaled urban particles. Transcript levels were measured using high density microarrays in total RNA isolated from whole lungs of wildtype and TNF-α overexpressing mice exposed by inhalation to particulate matter and euthanized immediately or 24 h post-exposure. Experiment Overall Design: Transgenic SP-C/TNF-α mice and their wildtype littermates were exposed by inhalation to particulate matter (0, 42 mg/m3 EHC-93) for 4 h and euthanized immediately or 24 h post-exposure (n=5 per treatment per time point, 40 animals total). Agilent 22K oligonucleotide microarrays were used to examine transcript levels in whole lung RNA. Stratagene Universal Mouse RNA was used as a reference.
2009-03-28 | E-GEOD-11037 | biostudies-arrayexpress
Project description:We examined the impact of chronic lung inflammation on the pulmonary transcriptional response to inhaled urban particles. Transcript levels were measured using high density microarrays in total RNA isolated from whole lungs of wildtype and TNF-α overexpressing mice exposed by inhalation to particulate matter and euthanized immediately or 24 h post-exposure. Keywords: Toxicology, disease state analysis, stress response
2009-03-23 | GSE11037 | GEO
Project description:A complete understanding of how environmental carcinogenic exposures promote cancer formation is lacking. Over 70 years ago, tumour formation was proposed to occur in a two step process: an initiating step which induces mutations in normal tissue, followed by a promoter step which triggers cancer development. Recent evidence has revealed healthy human tissue contains a patchwork of clones harbouring oncogenic mutations.This led us to hypothesise that environmental particulate matter measuring PM2.5, known to be associated with lung cancer risk, might promote lung cancer by acting on pre-existing cells harbouring oncogenic mutations in normal lung tissue. Here we use a combination of WGS and RNA-seq of mouse tumours from pollution-exposed mice to examine the impact of particulate matter on mutagenesis and gene expression respectively.
| EGAS00001006951 | EGA
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.
2009-08-10 | GSE17478 | GEO
Project description:We hypothesize that gene expression in the cigarette smoke (CS) exposed neonatal lung and age-matched controls will be divergent. CS exposed lung will have divergence of immune response genes and structural genes. The lungs of (6) 2 week old neonatal mice exposed to 2 weeks of CS were compared to the lung of (4) 2 week old age-matched control mice. We utilized microarray analysis to examine transcriptional differences between smoke exposed neonatal lung and age-matched controls. Keywords: comparative expression profiling
2008-01-01 | GSE7310 | GEO
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
Project description:Rationale: Chronic obstructive pulmonary disease (COPD) is a prevalent respiratory disease lacking disease modifying treatment. The role of CXCL12/CXCR4 axis has been demonstrated in acute exacerbation of COPD. The interest of study early COPD has been recently pointed out. Objectives: To study the role of the CXCL12/CXCR4 axis in both human and mouse model of early COPD. Methods: Blood and lung tissue were obtained from both COPD patients and mice exposed to cigarette smoke (CS) for 10 weeks and intranasal instillations of polyinosinic–polycytidylic acid (poly(I:C)) to mimic exacerbations for 5 weeks. Measurements and Main Results: Exposed mice presented mild airway obstruction, peri-bronchial fibrosis and right heart remodeling. The level of CXCR4 expressing cells was increased in the blood of exposed mice, as well as in the blood of patients with mild COPD. Lung CXCL12 expression was higher both in exposed mice and COPD patients. The densities of fibrocytes expressing CXCR4 were increased in the blood and in the bronchial submucosa of exposed mice. Conditional inactivation of CXCR4 at adult stage as well as pharmacological inhibition of CXCR4 with plerixafor injections improved lung function and inflammation and protected against CS and poly-(I:C)-induced airway and cardiac remodeling. CXCR4-/- and plerixafor-treated mice also had reduced levels of CXCR4-expressing circulating cells and a lower density of peri-bronchial fibrocytes. Conclusions: We demonstrated that targeting CXCR4 has beneficial effects in an animal model of early COPD, and provide a framework to translate preclinical findings to clinical settings within a drug repurposing approach.
2025-05-12 | PXD040105 | Pride
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) –induced 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. Keywords: gene expression
2007-12-01 | GSE9465 | GEO
Project description:These analyses set out to evaluate transcriptomic responses in the mouse lung and heart in response to simulated wildland fire exposure conditions. These exposure conditions were based on smoke condensate consisting of particulate matter and semivolative organic compounds resulting from the burning of five biomass fuels; namely eucalyptus, pine, pine needles, peat, and red oak. These biomasses were evaluated under two burn conditions: flaming and smoldering.
2022-09-01 | GSE164542 | GEO