Identification of exercise-related genes in mice exposed to cigarette smoke
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ABSTRACT:
PROVIDER: PRJEB56585 | ENA |
REPOSITORIES: ENA
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Project description:Cigarette smoke (CS) is the major risk factor for COPD and is linked to cardiopulmonary dysfunction. Exercise training, as part of pulmonary rehabilitation, is recommended for all COPD patients. It has several physiological benefits, but the involved mechanisms remain poorly defined. Here, we employed transcriptomic profiling and examined lung endothelium to investigate novel interactions between exercise and CS on cardiopulmonary alterations. Mice were exposed to 20 weeks of CS, CS + 6 weeks of high-intensity interval training on a treadmill or control. Lung and cardiac (left and right ventricle) tissue were harvested, and RNA-sequencing was performed and validated with RT-qPCR. Immunohistochemistry assessed pulmonary arteriolar changes. Transcriptome analysis between groups revealed 37 significantly regulated genes in the lung, 21 genes in the left ventricle, and 43 genes in the right ventricle (likelihood-ratio test). Validated genes that showed an interaction between exercise and CS included angiotensinogen (p=0.002) and resistin-like alpha (p=0.019) in left ventricle, with prostacyclin synthetase different in pulmonary arterioles (p=0.004). Transcriptomic profiling revealed changes in pulmonary and cardiac tissue following exposure to CS, with exercise training exerting rescue effects. Exercise-regulated genes included angiotensinogen and resistin-like alpha. However, it remains unclear if these represent potential candidate genes or biomarkers involved during pulmonary rehabilitation.
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Project description:hAEC cells were exposed to cigarette smoke extract (CSE) or PBS for 48h, and gene expression was evaluated by RNA-seq.In this study we explored the effect of cigarette smoke on the gene expression profile.
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Project description:Human alveolar epithelial cells were exposed to cigarette smoke extract (CSE) for 1, 3 and 5 weeks at 1%, 5% and 10%, and gene expression was evaluated by complete transcriptome microarrays. In this study we explored the effect of cigarette smoke on the gene expression profile.
2016-02-16 | GSE77942 | GEO
Project description:Gene expression patterns were assessed in normal human bronchial epithelial (NHBE) cells exposed to cigarette smoke from a reference cigarette (2R4F, University of Kentucky) and a typical American brand of "light" cigarettes ("Lights") in order to develop a better understanding of the genomic impact of tobacco exposure, which can ultimately define biomarkers that discriminate tobacco-related effects and outcomes in a clinical setting. NHBE cells were treated with whole cigarette smoke for 15 minutes and alterations to the transcriptome assessed at 2, 4, 8 and 24 hours post-exposure using high-density oligonucleotide microarrays. Keywords: time course, cigarette smoke exposure
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Project description:Mammalian females are born with a finite number of non-renewing primordial follicles, the majority of which remain in a quiescent state for many years. Due to their non-renewing nature, these “resting” oocytes are particularly vulnerable to xenobiotic insult, resulting in premature ovarian senescence and the formation of dysfunctional oocytes. In this study we characterised the mechanisms behind cigarette smoke induced ovotoxicity, which is characterised by primordial follicle depletion. C57BL/6 5 week old female mice were exposed to cigarette smoke five times per week, for 12-18 weeks using a custom-designed and purpose-built nose-only, directed flow inhalation and smoke-exposure system. This was done in the hopes of gaining a better understanding of the mechanisms underpinning cigarette smoke induced ovotoxicity.
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Project description:Mycbacterium tuberculosis was exposed to cigarette smoke condensate (CSC) in 7H9 dextrose culture media. The transcriptional response to cigarette smoke condensate was compared to that of exposure to the CSC diluent, DMSO..
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Project description:In the context of male reproductive health, epidemiological studies have observed reduced testis size and abnormal sperm counts and morphology in adult men exposed in utero, although these findings are not always repeated. The ambiguity of these reports is confounded by a lack of controlled animal studies investigating the effects of maternal cigarette smoke exposure on male offspring reproductive health. In this study we examined the effects of cigarette induced reproductive toxicity on male offspring exposed during the gestational and weaning period using our novel direct nasal exposure mouse model of cigarette smoke-induced chronic obstructive pulmonary disease and female subfertility. This was done too gain a better understanding of the adverse effects of gestational maternal smoking on male offspring fertility.
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Project description:How LTβR-signalling drives chronic tissue damage particularly in the lung, which mechanisms regulate this process, and whether LTβR-blockade might be of therapeutic value has remained unclear. To study the mechanisms underlying LTβR-inhibition, a transcriptional analysis was performed on lung tissue from B6 mice exposed to cigarette smoke for 6 months and treated therapeutically with LTβR-Ig from 4 to 6 months compared to mice exposed to cigarette smoke for 6 months and treated with control Ig from 4 to 6 months and filtered air control. Single-cell RNA-Seq identified 24 distinct cell populations across >20,000 cells in lungs with distinct changes occurring upon cigarette smoke exposure and LTβR-Ig treatment.
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