Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA666452 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14018017.fastq.gz | Fastqsanger.gz | |||
| SRR14018018.fastq.gz | Fastqsanger.gz | |||
| SRR14018019.fastq.gz | Fastqsanger.gz | |||
| SRR14018020.fastq.gz | Fastqsanger.gz | |||
| SRR14018021.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 9 |
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Project description:Differential gene expression of cigarettes and electronic cigarettes
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Project description:Cigarette smoke is a major risk factor for the development and progression of chronic obstructive pulmonary disease. Tobacco smoking is also the main cause of lung cancer and the main preventable cause of other lung and heart disease. Strategies to eliminate cigarette smoking have led to the emergence of new tobacco-related products as alternatives for cigarette smoking or tools for smoking cessation. Electronic cigarettes (E-cigarettes) have been introduced to the market in recent years as an alternative to smoking conventional cigarettes. E-cigarettes are nicotine delivery devices by heating and converting to aerosol a liquid mixture composed of propylene glycol, vegetable glycerine, flavouring chemicals, and nicotine. Despite the lack of appropriate studies, e-cigarettes are nowadays widely used and advertised as safe cigarette replacements and the number of users is rapidly growing. Unlike cigarette smoke, where the determinant effects are well studied and documented, very limited amount of research has been done on the health effects and public health of e-cigarettes. The study aims to investigate the effects of e-cigarette vapour extract on gene expression in different primary isolated mouse lung cells [pulmonary arterial smooth muscle cells (PASMC) and alveolar epithelial type two cells (AECII)]. The cells will be exposed to e-cigarette vapour extract (ECVE).
2023-05-01 | GSE202215 | GEO
Project description:The emerging concern about chemicals in electronic cigarettes, even those without nicotine, de-mands the development of advanced criteria for their exposure and risk assessment. This study aims to highlight the sensitivity of lung nuclear receptors (NRs) to electronic cigarette e-liquids, independent of nicotine presence, and the influence of the sex variable on these effects.
2024-05-03 | GSE252208 | GEO
Project description:Electronic cigarettes (e-cigs) are battery-powered new tobacco products attracting wide attention due to their potential in promoting smoking cessation and uncertainty in long-term health effects. According to the scientific statement from the American Heart Association (AHA), e-cig use may be a potential threat to the cardiopulmonary system and populational studies suggested that e-cig aerosol could enhance arterial stiffness Laboratory evidence suggested that e-cigs could accelerate atherosclerosis and atherosclerosis or aortic aneurysm in mice, while the exact mechanisms of e-cig-related vascular effects remained largely unknown. Here, we investigate the sub-chronic effects of e-cig aerosol on vascular structure, function, and changes in single-cell transcriptome in mice.
2025-01-31 | GSE288003 | GEO
Project description:Background: While electronic cigarette (ECIG) use is rapidly rising, their safety profile remains uncertain. The effects of tobacco cigarette (TCIG) smoke on bronchial airway epithelial gene-expression have provided insights into tobacco-related disease pathogenesis. Understanding the impact of electronic cigarettes (ECIGs) on airway gene-expression could provide insights into their potential long-term health effects. Objectives: We sought to compare the bronchial airway gene-expression profiles of former TCIG smokers now using ECIGs with the profiles of former and current TCIG smokers. Methods: We performed gene-expression profiling of bronchial epithelial cells collected from TCIG smokers not using ECIGs (n=21), former smokers using ECIGs (n=15), and current TCIG smokers not using ECIGs (n=9). We then compared our findings with previous studies of the effects of TCIG use on bronchial epithelium, as well an in vitro model of ECIG exposure. Results: Amongst 3,165 genes whose expression varied between the three study groups (q < 0.05), we identified 468 genes significantly altered in ECIG users relative to former smokers (p < 0.05). 79 of these genes were up or down-regulated concordantly between ECIG and TCIG. We did not detect ECIG-associated gene expression changes in known pathways associated with TCIG usage. Genes downregulated in ECIG users are enriched among the genes most downregulated by exposure of airway epithelium to ECIG vapor in vitro. Conclusions: TCIG exposure was associated with a larger number of airway gene-expression changes than with ECIG exposures. ECIGs induce both distinct and shared patterns of gene expression relative to TCIGs in the bronchial airway epithelium.
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Project description:Smoking electronic cigarettes significantly alters the microbiome
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Project description:Electronic nicotine delivery system (E-Cigarette) use is prevalent among pregnant women. We examined whether E-Cigarette exposure impairs implantation. RNA microarray was performed on day 4.5 pseudopregnant mice exposed to E-Cigarettes or sham during each day of pregnancy.
2019-09-12 | GSE131077 | GEO
Project description:Electronic cigarette use has increased dramatically over the past three years, despite numerous reports of acute lung injury and even death. In this report we provide evidence from a nonhuman primate model for Electronic Vapor-Induced Lung Injury (EVALI), demonstrating significant lung pathology from electronic vaping (EV). Here we characterized the particle size and pathogenic effects induced by EV exposure of nonhuman primates using the commercial nicotine JUUL® pod modular devices. Vaping aerosols appear to preferentially and exclusively target the bronchioles while bypassing larger bronchi. We demonstrate a significantly smaller particle size, generated by the EV device relative to combustion product aerosols produced by conventional cigarettes. Histopathologically, vaping aerosols appear to preferentially and exclusively target the bronchioles while bypassing larger bronchi which is consistent with a significanlty smaller particle size compared to cigarette smoke. Our immunohistochemical and RNAseq studies provide further evidence for severe small airway inflammation and dysregulation of gene expression within immune cells derived from bronchial lavage, respectively. Our findings raise major concerns regarding the safety of e-cigarettes, and provide a mechanism for the preferential induction of lung injury by EV. Our results, in a species whose lung architecture is the closest possible approximation of that of a human adolescent, suggest the danger of the EV device itself and resultant small particulate aerosols produced, preferentially entering and damaging a highly susceptible part of the respiratory system.
2022-07-01 | GSE199072 | GEO
Project description:Although smoking cessation shows clear cardiovascular risk benefits, lung-related disease risk remains higher in former smokers than in never smokers. To better understand the factors involved in this phenomenon, ApoE-/- mice were exposed to mainstream cigarette smoke (CS) or a smoking cessation-mimicking protocol for up to six months. Analysis of bronchoalveolar lavage fluid (BALF) from CS-exposed ApoE-/- mice revealed the presence of high concentrations of mediators involved in functions ranging from inflammation to cell proliferation and tissue remodeling. Gene expression levels for many analytes found elevated in BALF were also increased in lung tissue, indicating that the inflammatory response was the result of local tissue activation and the contribution of recruited inflammatory cells. Gene set enrichment analysis (GSEA) of expression data from lungs of CS-exposed mice showed activation of pathways involved in cell proliferation and tissue remodeling and a progressive deactivation upon smoke exposure cessation. Distinct activation patterns of inflammation, complement, and xenobiotic metabolism pathways were found in nasal epithelium and lung parenchyma during CS exposure and smoking cessation. Exposure of ApoE-/- mice to CS for up to 6 months induced adaptive and inflammatory responses in the respiratory tract that were partially deactivated upon cessation. We were able to reveal molecular perturbations accompanying these changes during CS exposure and cessation. Differential CS-mediated responses of pulmonary and nasal tissues reflect common mechanisms but also the varying degrees of epithelial functional specialization along the respiratory tract. These findings provide novel clues for the identification of markers of COPD progression.
2013-10-19 | E-MTAB-1390 | biostudies-arrayexpress