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E-GEOD-36810

ABSTRACT: Expression data from mouse lungs exposed in-utero and/or as an adult to second-hand smoke (SHS)

OTHER RELATED OMICS DATASETS IN: PRJNA156921

PROVIDER: E-GEOD-36810 | ExpressionAtlas | 2015-09-28

REPOSITORIES: ExpressionAtlas

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Dataset's files

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			Action	DRS
	E-GEOD-36810-analysis-methods.tsv	Tabular
	E-GEOD-36810-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-36810-configuration.xml	Xml
	E-GEOD-36810-percentile-ranks.tsv	Tabular
	E-GEOD-36810.condensed-sdrf.tsv	Tabular

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Mus musculus

Project description:Expression data from mouse lungs exposed in-utero and/or as an adult to second-hand smoke (SHS)

| PRJNA156921 | ENA

Expression data from mouse lungs exposed in-utero and/or as an adult to second-hand smoke (SHS)

Project description:Second-hand smoke (SHS) exposure during pregnancy has adverse effects on offspring. We used microarrays to characterize the gene expression changes caused by in-utero exposure and adult exposure to SHS in adult mouse lungs. Left lungs from Balb/c male mice were collected at 15 weeks of age for RNA extraction and hybridization on Affymetrix mouse 430 2.0 microarrays. Based on their smoke exposure status, there are 4 groups of mice, each exposed in-utero to filtered-air or SHS and as an adult to filtered-air or SHS. We extracted RNA from 4 animals from each group for microarray analysis (N = 16 samples).

2012-03-26 | E-GEOD-36810 | biostudies-arrayexpress

Dissecting the molecular effects of cigarette smoke on proteasome function

Project description:Proteasome dysfunction is emerging as a novel pathomechanism for the development of chronic obstructive pulmonary disease (COPD), a major leading cause of death in the world. Cigarette smoke is one of the main risk factors for COPD and has been shown to impair proteasome function in vitro and in vivo. Importantly, proteasome activity is inhibited in COPD lungs while expression levels of proteasome subunits are not altered. In the present study, we dissected the molecular changes induced by cigarette smoke on proteasome function in lung epithelial cells and mouse lungs. We analyzed the integrity, composition, and the interactome of isolated 26S proteasome complexes from smoke-exposed cells and mouse lungs. Moreover, we applied native MS analysis to investigate whether reactive compounds of cigarette smoke directly modify and inhibit the 20S proteasome complex. Our data reveal that the 20S proteasome is slightly destabilized in the absence of any dominant modification of proteasomal proteins. 26S pulldown and stoichiometry analysis indicated that 26S proteasome complexes become instable in response to cigarette smoke exposure. Of note, the interactome of the 26S was clearly altered in smoke-exposed mouse lungs possibly reflecting an altered cellular composition in the lungs of the smoke-exposed mice. Taken together, our results suggest that cigarette smoke induces minor but detectable changes in the stability and interactome of 20S and 26S proteasome complexes which might contribute in a chronic setting to imbalanced proteostasis as observed in chronic lung diseases associated with cigarette smoking.

2019-01-08 | PXD007148 | Pride

Expression data from mouse lungs exposed in-utero and/or as an adult to second-hand smoke (SHS)

2012-03-27 | GSE36810 | GEO

Mus musculus

Project description:Expression data from mouse lungs, exposed in-utero to second-hand smoke (SHS) and challenged with ovalbumin (OVA) as adults.

| PRJNA167827 | ENA

E-GEOD-38409

Project description:Expression data from mouse lungs, exposed in-utero to second-hand smoke (SHS) and challenged with ovalbumin (OVA) as adults.

2015-09-28 | E-GEOD-38409 | ExpressionAtlas

Mus musculus

Project description:Expression data from adult mouse testis exposed to cigarette smoke in utero

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Mus musculus

Project description:Expression data from adult mouse ovaries exposed to cigarette smoke in vivo

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Lung miRNA expression profiling in a mouse model of chronic obstructive pulmonary disease

Project description:To profile lung miRNA expression in our mouse model of cigarette smoke-induced chronic obstructive pulmonary disease, we employed the Agilent unrestricted Mouse miRNA (8 x 15k arrays per slide, AMADID Number: 021828, Sanger Version 12) platform as a discovery tool to identify miRNAs of interest in the development of experimental chronic obstructive pulmonary disease. Mice were exposed to cigarette smoke (or room air) for 4, 6, 8, 12 weeks, lungs were excised, and total RNA isolated.

2021-11-05 | GSE186955 | GEO

Transcription profiling of mouse C57BL6J lung exposed to 2 weeks of cigarette smoke compared to age-matched controls

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. Experiment Overall Design: This study utilizes microarray analysis to test these hypotheses. Six sets of lungs were harvested from CS exposed mice and four sets of lungs were harvested from age-matched control mice. RNA was isolated and used for global gene expression profiling (Affymetrix Mouse 430 2.0 array). Statistically significant gene expression was determined as a minimum 6 counts of 9 pairwise comparisons, minimum 1.5-fold change, and p < 0.05. Further, Absolute | FC - FC SEM | >= 1.5.

2008-06-15 | E-GEOD-7310 | biostudies-arrayexpress

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