Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptome analysis of Cox4-2 knockout mice after OVA challenge

ABSTRACT: Cytochrome c oxidase (COX) is a 13-subunit enzyme that is a key complex of the oxidative phosphorylation system of the mitochondria, which generates the vast majority of the energy of the cell.COX subunit IV is the largest nuclear-encode subunit with important regulatory functions concerning energy metabolism. COX4-2 has been knocked out. Our study indicated strong expression of Cox4-2 in lung and therefore we test this mutant line under OVA-challenge conditions expecting a new asthma mouse model. Total RNA obtained from 1/2 lung of 4 female mice of each analysed group (widltype, wildtype challenged, mutant, mutant challenged)

ORGANISM(S): Mus musculus

SUBMITTER: Martin Irmler

PROVIDER: E-GEOD-49694 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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 Âµm) 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 naÃ¯ve 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

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Transcriptome analysis of Cox4-2 knockout mice after OVA challenge

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