Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-18344
PROVIDER: PRJNA118151 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Cigarette smoke (CS) imposes a strong oxidative burden on exposed tissues resulting in a severely disturbed oxidant/antioxidant balance, which in the context of chronic exposure is assumed to be a key contributor to CS-related diseases. Because of its emerging central role in orchestrating the general cellular antioxidant response, the pathway leading to the activation of the transcription factor Nrf2 has received mounting attention over the past decade in investigations aimed at elucidating CS-induced patho-physiological mechanisms. To comprehensively characterize the impact of Nrf2 in acute and sub-chronic smoking scenarios, Nrf2 knock-out mice and their wildtype ICR littermates were exposed to either ambient air (sham exposure) or to one of three doses of CS for up to 5 months with two post-exposure endpoints of 1 and 13 days. The lungs of the mice were monitored for transcriptomic changes on a genome-wide level. 110 samples from 28 different groups are analyzed. For each group there are 4 replicates, besides two groups with only 3 replicates. Group parameteres are: genotype (WT, KN), treatment (sham, smoke), dosage of smoke treatment (low, medium, high), time of smoke treatment (1 day, 2 month, 5 month, 5 month + 1 day recovery, 5 month + 13 days recovery)
2010-02-27 | E-GEOD-18344 | biostudies-arrayexpress
Project description:Background and Aims: The impact of cigarette smoke on inflammatory bowel disease has been established by a large number of epidemiological, clinical, and preclinical studies. Exposure to cigarette smoke is associated with a higher risk of developing Crohn’s disease but is inversely correlated with the development, disease risks, progression, and relapse rate of ulcerative colitis. Few mechanistic studies have investigated the effect of cigarette smoke on intestinal inflammation and microbial composition. Methods: Three groups of mice were exposed to three different concentrations of cigarette smoke for a total of 4 weeks, including 5 days of dextran sulfate sodium treatment to induce colitis and a 7-day recovery period. A comprehensive and integrated comparative analysis of the global colon transcriptome and microbiome, as well as classical endpoints, was performed. Results: Cigarette smoke exposure significantly decreased the severity induced colitis. Colon transcriptome analysis revealed that cigarette smoke downregulated specific pathways in a concentration-dependent manner, affecting both the inflammatory state and composition of the gut microbiome. Metagenomics analysis demonstrated that cigarette smoke can modulate dextran sulfate sodium-induced dysbiosis of specific bacterial genera, contributing to resolve the inflammation or accelerate recovery. Conclusions: Cigarette smoke alters gut microbial composition and reduces inflammatory responses in a concentration-dependent manner. The present study lays the foundation for investigating potential molecular mechanisms responsible for the attenuation of colitis by cigarette smoke.
2020-03-03 | E-MTAB-7988 | biostudies-arrayexpress
Project description:We have investigated the effects of cigarette smoke exposure in three different strains of mice. DBA/2 and C57Bl/6J are susceptible to smoke and develop different lung changes in response to chronic exposure, while ICR mice are resistant to smoke and do not develop emphysema. The present study was carried out to determine early changes in the gene expression profile of mice exposed to cigarette smoke with either a susceptible or resistant phenotype.
2008-07-10 | GSE12036 | GEO
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
Project description:Diet-Induced Obesity Exacerbates Inflammatory and Oxidative Stress Responses in Mice Exposed to Cigarette Smoke
| PRJNA167200 | ENA
Project description:Gene expression data on wild-type and Rora mutant mice exposed to room air and smoke. The results provide a general insight into the relationship of Rora to known DNA damage response pathways and its role in cigarette smoke-induced airspace enlargement. This dataset includes 4 wild-type mice exposed to room air, 4 wild-type mice exposed to cigarette smoke and 4 Rora mutant mice exposed to cigarette smoke.
2012-07-22 | E-GEOD-33512 | biostudies-arrayexpress
Project description:We have investigated the effects of cigarette smoke exposure in three different strains of mice. DBA/2 and C57Bl/6J are susceptible to smoke and develop different lung changes in response to chronic exposure, while ICR mice are resistant to smoke and do not develop emphysema. The present study was carried out to determine early changes in the gene expression profile of mice exposed to cigarette smoke with either a susceptible or resistant phenotype. Experiment Overall Design: Three strains of mice were exposed to smoke from three cigarette/day, 5d/wk for 4 weeks. Microarray analysis was carried out on total RNA extracted from the lung utilizing the Affymetrix platform.
2008-10-21 | E-GEOD-12036 | biostudies-arrayexpress
Project description:Cigarette smoke (CS) imposes a strong oxidative burden on exposed tissues resulting in a severely disturbed oxidant/antioxidant balance, which in the context of chronic exposure is assumed to be a key contributor to CS-related diseases. Because of its emerging central role in orchestrating the general cellular antioxidant response, the pathway leading to the activation of the transcription factor Nrf2 has received mounting attention over the past decade in investigations aimed at elucidating CS-induced patho-physiological mechanisms. To comprehensively characterize the impact of Nrf2 in acute and sub-chronic smoking scenarios, Nrf2 knock-out mice and their wildtype ICR littermates were exposed to either ambient air (sham exposure) or to one of three doses of CS for up to 5 months with two post-exposure endpoints of 1 and 13 days. The lungs of the mice were monitored for transcriptomic changes on a genome-wide level.
2010-02-06 | GSE18344 | GEO
Project description:Our previous study showed that AKR and C57BL/6 mice to cigarette smoke increased lipopolysaccharide (LPS)- induced increased lung vascular permeability. Viremic AKR mice were more susceptible to LPS-induced ALI than C57 on prolonged exposure. In this study we compared the global gene expression patterns to determine the genetic basis for the strain dependent responses to cigarette smoke and LPS-induced ALI. We found AKR transcriptomic responses didnot overlap with C57 mice and AKR mice showed increased responses compared to C57 mice. Global gene expression analysis using microarray was used to dermine the mechanisms of strain dependent responses to cigarette smoking and LPS mediated ALI
2023-05-28 | GSE193958 | GEO