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Expression data of lung tissues from ICR mice treated with or without single-walled carbon nanotubes (SWCNTs)

ABSTRACT: The SWCNTs can induce airway hyper-responsiveness (AHR) and chronic obstructive pulmonary disease (COPD)-like changes in mice model. The SWCNTs can induce clusters of proteinases, chemokines/cytokines, and macrophage receptors triggered signaling, which might play critical roles in the SWCNTs-induced pathological changes, including chronic inflammation and tissues remodeling. We used microarrays to detail the global programme of gene expression underlying and identified distinct classes of up-regulated genes during this process.

ORGANISM(S): Mus musculus

PROVIDER: GSE22856 | GEO | 2011/07/09

SECONDARY ACCESSION(S): PRJNA128065

REPOSITORIES: GEO

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Expression data of lung tissues from ICR mice treated with or without single-walled carbon nanotubes (SWCNTs)

Project description:The SWCNTs can induce airway hyper-responsiveness (AHR) and chronic obstructive pulmonary disease (COPD)-like changes in mice model. The SWCNTs can induce clusters of proteinases, chemokines/cytokines, and macrophage receptors triggered signaling, which might play critical roles in the SWCNTs-induced pathological changes, including chronic inflammation and tissues remodeling. We used microarrays to detail the global programme of gene expression underlying and identified distinct classes of up-regulated genes during this process. Lung tissues from adult ICR mice (6 weeks old) treated with or without single dose of 0.5 mg SWCNTs by intratrachael instillation were collected and homogenated under liquid nitrogen for RNA extraction and hybridization on Affymetrix microarrays. Since our data showed that the SWCNTs could induce significantly pulmonary granuloma and COPD-like lesion. Two time points of the samples have been collected for microarray analysis: day 1 after SWCNTs treatment as the acute phase responses; day 7 as the sub-chronic responses. We tried to compare the SWCNTs-regulated gene expression profiles with the PF68-treated (as the solvent control) to identify the possible mechanisms of SWCNTs-induced toxicity in lung.

2011-07-09 | E-GEOD-22856 | biostudies-arrayexpress

Expression data from Caenorhabditis elegans exposed to single-walled carbon nanotubes

2012-10-11 | GSE41486 | GEO

Expression data from Caenorhabditis elegans exposed to single-walled carbon nanotubes

Project description:The potential environmental risk of single-walled carbon nanotubes (SWCNTs) is evaluated using Caenorhabditis elegans (C. elegans) as an ecotoxicological animal model. Highly soluble amide-modified SWCNTs (a-SWCNTs) are used in the present study so that the dose-response impact of SWCNTs could be studied. mechanisms. a-SWCNTs are efficiently taken up by worms during feeding and cause significant toxicity in worms, including retarded growth, shortened lifespan and defective embryogenesis. Genome-wide gene expression analysis is performed to investigate the toxic molecular We examined the effect of different concentrations of a-SWCNTs (0, 100, 250 and 500 Î¼g/mL) on the growth of C. elegans. We measured the body length of worms reaching the L4 stage after a-SWCNT exposure for 48 hr at 22Â°C. Compared to the untreated worms, we found that the average length of worms exposed to a-SWCNTs (500 Î¼g mL-1) was significantly shorter than the untreated groups. In addition, the dose of a-SWCNTs also caused retarded growth, reduced lifespan and defective embryogenesis in worms. Genome-wide gene expression analysis using an Affymetrix GeneChip was performed to further investigate the molecular basis of these defects.

2012-10-11 | E-GEOD-41486 | biostudies-arrayexpress

Exposure of human A549 and THP-1 cells and mouse J774 cells to single walled carbon nanotubes

Project description:The microarray investigations were part of a toxicological investigation of the effect of exposure to single-walled carbon nanotubes (SWCNTs) to macrophages and non-phagocytotic cells The results of this study are accepted for publication in Toxicological Research with the title: The toxic effects of single-wall carbon nanotubes are linked to the phagocytic ability of cells Cell lines were treated for 24 hours either with water (vehicle control) or SWCNTs for 24 hours and the toxic effects were investigated including gene expression changes by affymetrix microarrays.

2014-01-03 | E-GEOD-53765 | biostudies-arrayexpress

An environmental ecocorona influences the formation and evolution of the biological corona on the surface of single-walled carbon nanotubes - proteome

Project description:In this study, the formation of a protein corona on two different SWCNTs under presence or absence of an ecocorona was investigated at four different time points.

2021-04-14 | PXD022788 | Pride

Autoantibody profiles in patients with COPD and non-COPD smokers

Project description:Chronic obstructive pulmonary disease (COPD) is a highly prevalent disease leading to irreversible airflow limitation and is characterized by chronic pulmonary inflammation，obstructive bronchiolitis and emphysema. Etiologically, COPD is mediated by toxic gases and particles, e.g. cigarette smoke, while the pathogenesis of the disease is largely unknown. Several lines of evidence indicate a link between COPD and autoimmunity but comprehensive studies are lacking. By using a protein microarray assaying more than 19,000 human proteins we determined in this study the autoantibody profiles of COPD and non-COPD smokers.

2019-06-21 | GSE133096 | GEO

trancription profiling by array of human pulmonary and circulating CD8 cells in COPD

Project description:Background: CD8 cells seem to play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). However, relatively little is known about their phenotype and function. Aims: To define the transcriptome of pulmonary CD8 cells in COPD and compare to paired circulating CD8 cells and smoker control pulmonary CD8 cells. COPD was defined according to the Global initiative for chronic Obstructive Lung Disease guidelines. Severity of disease was defined according to the patients lung function. In particular the forced evpiratroy volume in 1 second (FEV1).

2013-08-01 | E-MTAB-1688 | biostudies-arrayexpress

Chronic obstructive pulmonary disease (COPD)

Project description:Chronic obstructive pulmonary disease (COPD) Metagenome

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Exposure of human A549 and THP-1 cells and mouse J774 cells to single walled carbon nanotubes

2014-01-03 | GSE53765 | GEO

MMP28 is a key contributor to emphysema pathogenesis

Project description:Chronic Obstructive Pulmonary Disease, which is comprised of chronic bronchitis and emphysema, is a leading cause of morbidity and mortality. Because tissue destruction is the prominent characteristic of emphysema, extracellular proteinases, particularly those with elastolytic ability, are often considered to be key drivers in this disease. Several human and mouse studies have implicated roles for matrix metalloproteinases (MMPs), particularly macrophage-derived proteinases, in COPD pathogenesis. MMP28 is expressed by the pulmonary epithelium and macrophage, and we have found that it regulates macrophage recruitment and polarization. We hypothesized that MMP28 would have contributory roles in emphysema via alteration of macrophage numbers and activation. Because of the established association of emphysema pathogenesis to macrophage influx, we evaluated the inflammatory changes and lung histology of Mmp28-/- mice exposed to 3 and 6 months of cigarette smoke. At earlier time-points, we found altered macrophage polarization in the smoke-exposed Mmp28-/- lung consistent with other published findings that MMP28 regulates macrophage activation. At both 3 and 6 months, Mmp28-/- mice had blunted inflammatory responses more closely resembling non-smoked mice, with a reduction in neutrophil recruitment and CXCL1 chemokine expression. By 6 months, Mmp28-/- mice were protected from emphysema. These results highlight a previously unrecognized role for MMP28 in promoting chronic lung inflammation and tissue remodeling induced by cigarette smoke and highlight another potential target to modulate COPD.

2017-02-18 | GSE93898 | GEO

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