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Mus musculus

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

OTHER RELATED OMICS DATASETS IN: E-GEOD-36810

PROVIDER: PRJNA156921 | ENA |

REPOSITORIES: ENA

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

2012-03-27 | GSE36810 | GEO

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

E-GEOD-36810

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

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

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

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

Project description:SHS exposure during pregnancy has adverse effects on offspring. We used microarrays to characterize the gene expression changes caused by in-utero SHS exposure and adult (19-23 weeks) OVA challenge in 23-week mouse lungs. Left lungs from Balb/c male and female mice were collected at 23 weeks of age for RNA extraction and hybridization on Affymetrix mouse 430 2.0 microarrays. Based on the gender differences and in-utero exposure status, there are 4 groups of mice, females and males, exposed in-utero to filtered-air or SHS. All were exposure to OVA (19-23 weeks). We extracted RNA from 4 animals from each group for microarray analysis (total N = 16 samples).

2012-06-01 | E-GEOD-38409 | biostudies-arrayexpress

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

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

2012-06-02 | GSE38409 | GEO

Secondhand smoke induces liver steatosis through deregulation of genes involved in lipid metabolism.

Project description:In this study, we have investigated the role of secondhand smoke (SHS) in the development of metabolic liver disease by characterizing the global regulation of genes and molecular pathways in SHS-exposed mice after termination of exposure (SHS 4M) and following one-month recovery in clean air (SHS 4M +1M RECOVERY).

2020-03-23 | GSE139440 | GEO

Mus musculus

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

| PRJNA223381 | ENA

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

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