Mouse study
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB26965 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2597590_1.fastq.gz | Fastqsanger.gz | |||
| ERR2597590_2.fastq.gz | Fastqsanger.gz | |||
| ERR2597600_1.fastq.gz | Fastqsanger.gz | |||
| ERR2597600_2.fastq.gz | Fastqsanger.gz | |||
| ERR2597610_1.fastq.gz | Fastqsanger.gz |
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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: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:Fibroblast growth factor (FGF) 10 is essential for lung morphogenesis and polymorphisms in the Fgf10 region are linked with higher susceptibility towards COPD in human patients. We found that FGF10 signaling is impaired in lung septal wall compartment from COPD patients. Mice with impaired FGF10 signaling (Fgf10+/-) were more prone to develop cigarette smoke (CS)-induced emphysema and pulmonary hypertension (PH). Furthermore, FGF10 overexpression could successfully reverse cigarette smoke-induced emphysema and PH in mice.
2024-04-01 | GSE230854 | GEO
Project description:NOXO1 KO mice seem to be protected from cigarette smoke-induced emphysema and pulmonary hypertension. Since the molecular mechanisms are not clear yet, this microarray experiment should help to identify the molecular differences in these KO mice compared to the wild-type (WT), figuring out how the protection occurs. Since we believe that vascular altertions could not only be responsible for vascular remodeling but also the trigger for emphysema development, we microdissected pre-capillary vessels from WT and KO mice, both controls and smoke-exposed. In addition, alveolar septa were microdissected to investigate the alveolar changes.
2020-03-01 | GSE112287 | GEO
Project description:Cigarette smoking causes serious diseases, including lung cancer, heart disease, and emphysema. While cessation remains the most effective approach to minimize smoking-related disease, alternative non-combustible tobacco-derived nicotine containing products may reduce disease risks among those unable or unwilling to quit. E-vapor aerosols typically contain significantly lower levels of smoke-related harmful and potentially harmful constituents; however, health risks of long-term inhalation exposures are unknown. We designed a 7-month inhalation study in C57BL/6 mice to evaluate long-term respiratory toxicity of e-vapor aerosols compared to cigarette smoke and to assess the impact of smoking cessation or switching to an e-vapor product after 3 months of exposure to 3R4F cigarette smoke (CS). There were no significant changes in in-life observations (body weights, clinical signs) in e-vapor groups compared to the Sham Control. The 3R4F CS group showed reduced respiratory function during exposure and had lower body weight and showed transient signs of distress post-exposure. Following 7 months of exposure, e-vapor aerosols resulted in no or minimal increase in pulmonary inflammation, while exposure to 3R4F CS led to impairment of lung function and caused marked lung inflammation and emphysematous changes. Biological changes observed in the Switching group were similar to the Cessation group. 3R4F CS exposure dysregulated lung and nasal tissue transcriptome, while these molecular effects were substantially lower in the e-vapor group. Results from this study demonstrate that in comparison with 3R4F CS, e-vapor aerosols induce substantially lower biological responses including pulmonary inflammation and emphysema, and that complete switching from CS to e-vapor products significantly reduces biological changes associated with cigarette smoke in C57BL/6 mice.
2021-03-18 | E-MTAB-9597 | biostudies-arrayexpress
Project description:The lymphatic vasculature is critical for lung function, but defects in lymphatic functionin the pathogenesis of lung disease is understudied. To further assess the contribution of lymphatics to the pathogenesis of lung emphysema we used a mouse model of cigarette smoke (CS)-induced emphysema, and analyzed lung lymphatics using immunohistochemistry, functional assays, and confocal microscopy. Additionally, we further harvested thoracic lymph from CS-exposed mice for proteomic analysis. In this presented section of our research, we highlight the label free quantitative DIA proteomics approaches used to profile the proteomic and peptidomics changes in the lymph from cigarette smoke (CS)-mice as compared with the lymph proteome from mice exposed to room air. Label free quantitative DIA proteomics analysis of lymph confirmed upregulation of coagulation and inflammatory pathways in the lymphatics of CS-exposed mice compared to control mice.
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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: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.
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Project description:Chymotrypsin-like elastase 1 (CELA1) is a serine protease that is neutralized by alpha-1 antitrypsin (AAT) and prevents emphysema in a murine antisense oligonucleotide model of AAT-deficient emphysema. We tested the role of CELA1 in emphysema development in this genetic model of AAT-deficiency following tracheal lipopolysaccharide (LPS), 10 months of cigarette smoke (CS) exposure, aging, and a low-dose tracheal porcine pancreatic elastase (LD-PPE) model we developed. In this last model, we performed proteomic analysis to understand differences in lung protein composition. We were unable to show that AAT-deficient mice developed more emphysema than wild type with escalating doses of LPS.
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Project description:Emphysema is a unique type of chronic obstructive pulmonary disease, and sex may influence susceptibility. After cigarette smoke exposure, murine males and ovariectomized females developed more severe emphysema. Herein, we present divergent bulk and single-cell transcriptomic profiles between male and female murine lungs. Weighted Gene Co-Expression Network Analysis of the bulk lung RNA sequencing identified a Green gene module that correlated with male sex and ovariectomy. The Green gene module was enriched in common monocyte progenitors, classical monocytes, type 1 dendritic cells, and macrophages from 83,698 murine cells exposed to air or cigarette smoke for five months. Sexual dimorphism altered the compositions and transcriptome of the clusters enriched with the Green gene module. This comprehensive transcriptomic analysis advances our understanding of dynamic cellular responses controlled by sexual dimorphism during the development of emphysematous pulmonary tissue remodeling and reveals potential targets for mechanistic studies in the future.
2022-05-31 | GSE200587 | GEO