Gene expression signature induced by 8 weeks of cigarette smoke exposure in the lung of BALB/c mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE55127 | GEO | 2014/04/01
SECONDARY ACCESSION(S): PRJNA238586
REPOSITORIES: GEO
Similar Datasets
Project description:To investigate the impact of cigarette smoke on lung gene expression, female BALB/c mice were obtained from Charles River at 6-8 weeks of age. Using a whole body exposure system (SIU48, PROMECH LAB AB, Vintrie, Sweden), mice (5 per group) were exposed to room air or the mainstream cigarette smoke of twelve 3R4F reference cigarettes (University of Kentucky, Lexington, USA) with filters removed 5 days per week, twice daily for 50 minutes/exposure for 8 weeks, as previously described. Control animals were exposed to room air only. Lungs were collected and stored in RNALater at -80M-BM-0C prior to RNA extraction. Impact of an 8 week cigarette smoke exposure on BALB/c mouse lung gene expression was assessed.
2014-04-01 | E-GEOD-55127 | biostudies-arrayexpress
Project description:These studies tested the hypotheses that smoke induces changes in mRNA profiles that are dependent on sex and the health status of the lung, and that the effects of smoke are different after 1 day compared to 5 days of smoke exposure. The ways in which the lungs modulate their response to cigarette smoke after repeated exposures are important for understanding the toxicology of smoke, for developing biomarkers of chronic smoke exposure, and for understanding the therapeutic potential in regulatory signaling pathways that are beneficial or detrimental to lung health. Sex-matched 5-7-week old wildtype (WT) and Scnn1b-overexpressing (BENaC) littermates were exposed to cigarette smoke or sham (room air) exposure. Exposure occurred in a plexiglass chamber attached to a smoke delivery device using an exposure chamber and smoking machine (inExpose Exposure System, SCIREQ, Chandler, AZ). Mice were exposed to mainstream + sidestream smoke from 6 reference cigarettes with filters removed per day (3R4F research cigarettes, University of Kentucky). Each cigarette was puffed for 2 sec every 25 sec, using the standard Federal Trade Commission smoking machine protocol. The sham-exposed control mice were exposed to room air in the exposure chamber for a time equivalent to that needed for active smoke exposure. Mice were exposed to cigarette or sham smoke for 1 day or 5 consecutive days. Samples were harvested 4 hours after the completion of the final smoke exposure. The right lung was used for gene expression analysis.
2019-03-18 | GSE109776 | GEO
Project description:A 7-month inhalation study in C57BL/6 mice was conducted 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). In this study, we performed a chronic inhalation (4 h/day, 5 d/week, up to 7 months) study in C57BL/6 mice using a commercial (MarkTen®) e-vapor product and a combustible reference cigarette (3R4F) using a Switching and Cessation study design. A commercial e-vapor product (MarkTen® device [version 2.6.8]; “Test Red”) was supplied by Altria Client Services LLC (Richmond, VA, USA). The Test Red formulation was composed of aerosol formers (propylene glycol [PG] and vegetable glycerol [VG]), ~4% nicotine by weight, and flavors (non-menthol). The 3R4F commercial reference cigarettes were purchased from the University of Kentucky (Lexington, KY). HEPA filtered air at the testing facility (Battelle, West Jefferson, OH) was used as Sham Control. General procedures for animal care and housing met the Association for Assessment and Accreditation of Laboratory Animal Care (AAALAC) recommendations and requirements stated in the “Guide for Care and Use of Laboratory Animals” [National Research Council (NRC)] and approved by the Institutional Animal Care and Use Committee (IACUC). Female C57BL/6 mice were received from Charles River Kingston (Stone Ridge, NY). Test atmosphere was generated from smoking machines and delivered to the mice through a nose-only exposure system. The modified Cooperation Centre for Scientific Research Relative to Tobacco (CORESTA) Reference Method 81 regimen (55/30/5: a 55 ± 0.3 mL puff volume, a puff every 30 seconds, a 5-second puff duration) was used to generate e-vapor aerosol for 130 puffs/cartridge. Mainstream smoke from 3R4F cigarette was generated using a modified Health Canada Intense regimen (55/30/2: a 55 ± 0.3 mL puff volume, a puff every 30 seconds, a 2-second puff duration, and a near-square puff profile) for 8 puffs/cigarette. Female C57BL/6 mice (~10 weeks old) were randomly assigned based on body weight to one of five exposure groups: Sham Control, 3R4F CS, Test Red, Switching, and Cessation. Mice were exposed to 3R4F CS (550 µg/L TPM) or e-vapor aerosols (Test Red; 1100 µg/L TPM) via nose-only inhalation up to 4 h/day, 5 d/week for up to 7 months. After the first 3 months of exposure, groups of 3R4F CS mice were subjected to exposures of: (1) Test Red aerosol (“Switching”) or (2) filtered air (“Cessation”), while a group of mice continued to be exposed to 3R4F CS. Here, the protein expression data for lung tissue assessed by iTRAQ®-based quantitative proteomics is reported.
2021-03-31 | PXD019918 | Pride
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. C57BL/6 5 week-old female mice were exposed via the nose-only to cigarette smoke [twelve 3R4F reference cigarettes (University of Kentucky, USA) twice/day, five times per week, for 12-18 weeks]. Each exposure lasted 60 minutes. Control mice received room air. In total, 27 mice underwent cigarette smoke exposure. Eleven week-old female mice exposed to cigarette smoke for 6 weeks were separated into groups of three and housed with a single control stud male aged 7-8 weeks with proven fertility for a maximum of 12 weeks. Females were monitored every second day for post-coital plugs and pregnancy. Pregnant females were separated into single cages and litter sizes/pup weights recorded. Smoke exposure via dams continued throughout mating/pregnancy/lactation until weaning of pups at 21days post birth. The testis of exposed offspring were then collected for RNA extraction and hybridization on an Illumina Sentrix Mouse ref-8 v2 Beadchip
2013-10-23 | E-GEOD-51530 | biostudies-arrayexpress
Project description:To profile lung miRNA expression in our mouse model of cigarette smoke-induced chronic obstructive pulmonary disease, we employed the Agilent unrestricted Mouse miRNA (8 x 15k arrays per slide, AMADID Number: 021828, Sanger Version 12) platform as a discovery tool to identify miRNAs of interest in the development of experimental chronic obstructive pulmonary disease. Mice were exposed to cigarette smoke (or room air) for 4, 6, 8, 12 weeks, lungs were excised, and total RNA isolated.
2021-11-05 | GSE186955 | GEO
Project description:Cigarette smoke (CS) is an aerosol containing more than 6,000 chemicals and one of the risk factor in the development of chronic inflammatory lung disease. To evaluate biological effect of CS on human respiratory tract, organotypic bronchial epithelial cultures can be used to replicate in vivo tissue conditions. The MucilAir organotypic bronchial epithelial cultures were exposed to mainstream aerosols from the 3R4F cigarette and a novel tobacco vapor product (NTV), which we recently developed, using a Vitrocell exposure system. This system consists of three steps: the generation of CS, dilution, and exposure to an air-liquid interface cultured cells in a specially designed module. This exposure scenario mimics CS exposure in the human airway (i.e. direct aerosol exposure to the apical surface of air-liquid interface-cultured cells), We found a dose-dependent increase in the number of differentially expressed genes following 3R4F cigarette smoke exposure, compared with expression in air-exposed controls. In contrast, no changes were detected following exposure to NTV vapor.
2018-02-09 | E-MTAB-6471 | biostudies-arrayexpress
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 M-bM-^@M-^\restingM-bM-^@M-^] 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. C57BL/6 5 week old female mice were exposed to cigarette smoke (twelve 3R4F reference cigarettes (University of Kentucky, USA) twice/day, 2.7 mg particulate matter) five times per week, for 12-18 weeks using a custom-designed and purpose-built nose-only, directed flow inhalation and smoke-exposure system. Their ovaries were then collected for RNA extraction and hybridization on an Illumina Sentrix Mouse ref-8 v2 Beadchip
2012-12-13 | E-GEOD-42889 | biostudies-arrayexpress
Project description:COPD is a disorder characterized by the progressive development of airflow limitation that is not fully reversible. Cigarette smoke has been generally accepted as the most important of many risk factors for the development of COPD. We used microarray technology to perform comprehensive gene expression profiling of smoke exposure and cessation effects in mouse muscle tissue. Mice received nose-only exposure of 4% mainstream cigarette smoke or air (sham exposure) for 2 hours/day, 5 days/week for 2, 12 or 24 weeks. Mice undergoing smoke cessation received cigarette smoke exposure for 12 weeks, and then sham exposure for 12 weeks.
2012-09-01 | E-GEOD-18033 | biostudies-arrayexpress
Project description:Single cell RNA-sequencing (scRNAseq) of lung immune cells from mice exposed to room air or cigarette smoke, infected with influenza A virus. Room air saline controls are also included. This analysis facilitates a comparison of cigarette smoke-associated changes to the pulmonary immune environment at the level of individual leukocytes and stromal cells.
2022-01-03 | GSE186976 | GEO
Project description:We found that mainstream cigarette smoking (4 cigarettes/day, 5 days/week for 6 weeks using Kentucky Research Cigarettes 3R4F) resulted in >20% decrease in the percentage of normal Paneth cell population in Atg16l1 T300A mice but showed minimal effect in wildtype littermate control mice, indicating that Atg16l1 T300A polymorphism confers sensitivity to cigarette smoking-induced Paneth cell damage. We performed transcriptional profiling to identify molecular mechanisms associated with Paneth cell defect in Atg16l1 T300A mice exposed to cigarette smoking. Female mice were used at 4-5 weeks of age. Cigarette smoking was performed using smoking chamber with the dosage and schedule as described above. The whole ileum of the mice were harvested for transcriptomic analysis after completing 6 weeks of smoking.
2018-10-31 | E-MTAB-5707 | biostudies-arrayexpress