Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA128635 | ENA |
REPOSITORIES: ENA
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Project description:Previous studies have shown that smoking induces oxidative stress and inflammation, known factors that coincide with the development and progression of silicosis. Nevertheless, the precise role of cigarette smoke exposure in silicosis and the underlying mechanisms are not clearly understood. Therefore, the objective of the present study was to determine the effect of smoking, if any, on silica-induced pulmonary response and the underlying mechanisms. Pulmonary toxicity and lung gene expression profiles were determined in male Fischer 344 rats exposed to air, crystalline silica, cigarette smoke or cigarette smoke plus crystalline silica. Silica exposure resulted in significant pulmonary toxicity which was further exacerbated by cigarette smoke exposure in the rats. Significant differences in the gene expression profiles were detected in the lungs of the rats exposed to cigarette smoke, silica or a combination of both compared with the control rats.
2020-11-01 | GSE136945 | GEO
Project description:Gene expression profiles in lung tissue of rats following exposure to mainstream cigarette smoke
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Project description:Synergism of Iraqi Sand/Cigarette Smoke Co-Exposure in Rats
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Project description:Expression data from rats exposed to cigarette smoke (CS) at three concentrations (sham, 300 µgTPM/l and 600 µgTPM/l) for 13 weeks (5d/week; 2hrs/day) after three different recovery times (2hrs, 6hrs and 20hrs after last treatment); lung tissue Keywords: recovery time course and dose dependency Male Sprague-Dawley rats were nose-only-exposed for 13 weeks in total, 5d/week, 2h/day to following concentrations of mainstream cigarette smoke from the standard reference cigarette 2R4F: sham, 300 µgTPM (Total particulate matter)/l or 600 µgTPM/l.
2006-07-27 | E-GEOD-4516 | biostudies-arrayexpress
Project description:Our previous studies have shown that tobacco smoke exposure exacerbated the lung response to crystalline silica exposure in rats. The objective of the present study, a follow-up to our previous study, was to determine the effect of tobacco smoke exposure cessation on the lung response to crystalline silica exposure in the rats. Rats were exposed to air, crystalline silica (1 week followed by a 1 year progression/recovery period with no exposure), tobacco smoke (6 months of exposure followed by 6 months of recovery with no exposure), or crystalline silica (1 week) plus tobacco smoke (6 months of exposure followed by 6 months of recovery with no exposure). Lung toxicity was determined at the end of the 1-year progression/recovery period in all 4 groups of the rats. Silica exposure resulted in significant lung toxicity which was further exacerbated by tobacco smoke exposure in the rats. Cessation of cigarette smoke exposure did not result in reversal of the silica-induced lung toxicity despite exacerbation of the toxicity by tobacco smoke.
2024-12-31 | GSE155924 | GEO
Project description:Skeletal muscle characteristics of inherited low and high aerobic exercise capacity
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Project description:Expression data from rats exposed to cigarette smoke (CS) at three concentrations (sham, 300µgTPM/l and 600µgTPM/l) for 13 weeks (5d/week; 2hrs/day) after three different recovery times (2hrs, 6hrs and 20hrs after last treatment); lung tissue Keywords: recovery time course and dose dependency
2006-07-28 | GSE4516 | GEO
Project description:<p>Background: Chronic obstructive pulmonary disease (COPD) is a progressive inflammatory disorder with rising global morbidity and mortality. Emerging evidence suggests that systemic metabolic alterations, particularly dyslipidemia, contribute to COPD pathogenesis. However, the mechanisms linking lipid dysregulation to pulmonary inflammation and tissue injury remain poorly defined.</p><p>Methods: Untargeted metabolomic profiling was performed on plasma samples from healthy individuals and patients with COPD to identify disease associated metabolic alterations. A high-cholesterol diet (HCD) mouse model, with or without chronic cigarette smoke exposure, was used to examine the impact of systemic cholesterol elevation on lung structure and inflammation. Complementary in vitro studies using THP-1 derived and bone marrow derived macrophages were conducted to investigate mitochondrial function, ROS generation, and downstream signaling pathways. Transcriptomic analyses were employed to identify key molecular mediators.</p><p>Results: Plasma metabolomics revealed significant dysregulation of lipid metabolism in COPD, with elevated cholesterol levels correlating inversely with lung function. In vivo, HCD feeding induced pulmonary inflammation and further exacerbated cigarette smoke induced lung tissue destruction. In macrophages, combined cholesterol loading and cigarette smoke extraction treatment disrupted mitochondrial integrity, reduced respiratory capacity, and increase ROS generation. Elevated ROS levels upregulated PPIA, which in turn activated NF-κB signaling and promoted IL-1β secretion. Silencing PPIA or inhibiting ROS significantly attenuated NF-κB activation and cytokine release. Consistent with these findings, increased PPIA expression and NF-κB phosphorylation were observed in lungs of HCD-fed, cigarette smoke exposed mice, and PPIA levels were elevated in bronchoalveolar lavage fluid from COPD patients.</p>
2025-11-26 | MTBLS13388 | MetaboLights
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