Cigarette smoke but not novel tobacco vapor product cause epigenetic disruption and cell apoptosis.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA660351 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12551068_1.fastq.gz | Fastqsanger.gz | |||
| SRR12551068_2.fastq.gz | Fastqsanger.gz | |||
| SRR12551069_1.fastq.gz | Fastqsanger.gz | |||
| SRR12551069_2.fastq.gz | Fastqsanger.gz | |||
| SRR12551070_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Novel tobacco vapor product, generating vapor without combusting tobacco leaves, has been developed expecting the number and quantity of chemicals in the vapor of these products to be reduced compared to conventional combustible cigarettes. However, if the lower chemical levels correlate with lower toxicity remained to be clarified. Here we examined the difference of conventional cigarette smoke (CS) and novel tobacco vapor product (NTV) using cultured cancer cell line A549 and normal bronchial epithelium cell line BEAS-2B. 0.5% of 3R4F which is conventional CS markedly decreased cell proliferation of both A549 and BEAS-2B, however Ploom TECH or Ploom TECH+ which are commercially available NTV did not affect cell growth. To clarify the cause of decreased cell proliferation, Tunnel assay was performed and clarified that apoptosis was observed in both A549 and BEAS-2B after 24hours after exposure to 3R4F. To further explore the effect of CS to epigenetics, we performed western blotting Histone H2A phosphorylation which is known to correlate transcriptional regulation. Only 3R4F decreased histone H2A phosphorylation of both A549 and BEAS-2B. Then we examined alterations of gene expression after 3R4F treatment of A549 cell. 339, 107, 103 genes which were upregulated more than 2fold were observed in 3R4F, Ploom TECH or Ploom TECH+ treated A549 cell, respectively. Among 339 genes which was upregulated 3R4F, we focused EGR1, FOS, and FOSB gene since they were upregulated more than100 fold. We confirmed this upregulation using RTqPCR. These data suggest that Cigarette smoke but not novel tobacco vapor product cause epigenetic disruption and cell apoptosis possibly by elevating genes such as EGR1.
2020-12-07 | GSE157165 | GEO
Project description:The current study was performed for analysis of the biological effects of vapor from novel tobacco vapor product in comparison with 3R4F cigarette smoke. This study was performed using a three-dimensional culture system composed of an air-liquid interface culture of primary normal human bronchial epithelial cells (MucilAir). The MucilAir tissues were subjected to 17 days of exposure to the aqueous extract of novel tobacco product vapor or 3R4F cigarette smoke. The number of differentially expressed genes increased in MucilAir tissues exposed to aqueous extract of each test product dependent on exposure duration. The number of differentially expressed genes was lower in the tissues exposed to aqueous extract of novel tobacco product vapor compared to the tissues exposed to aqueous extract of 3R4F cigarette smoke.
2020-04-15 | E-MTAB-8920 | biostudies-arrayexpress
Project description:Next generation product such as heat-not-burn type product and e-cigarette emit lower yields of chemical constituents than cigarette because combustion of tobacco leaves is not associated with their vapor generation. Therefore it is expected that the usage of these product bring beneficial impact on public health. However, risk-reduced potential as well as risk concerns in long-term use of these products has not yet been fully understood. In this study, we intended to estimate the risk reduced potential of our proprietary novel tobacco vapor product (NTV) by repeated exposure of in vitro 3D bronchial epithelial cells to NTV vapor in comparison with repeated exposure to cigarette smoke. In addition, to reflect the realistic situation of smokers, exposure switching from cigarette smoke to NTV vapor and cigarette smoke exposure cessation were conducted.
2020-03-31 | E-MTAB-8155 | biostudies-arrayexpress
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:We compared early biological changes in mice after inhalation exposures to cigarette smoke or e-vapor aerosols (MarkTen® cartridge with Carrier, Test-1, or Test-2 formulations; 4% nicotine). Female C57BL/6 mice were exposed to 3R4F cigarette smoke or e-vapor aerosols by nose-only inhalation for up to 4 hours/day, 5 days/week, for 3 weeks. The 3R4F and e-vapor exposures were set to match the target nose port aerosol nicotine concentration (∼41 µg/L). Only the 3R4F group showed postexposure clinical signs such as tremors and lethargy. At necropsy, the 3R4F group had significant increases in lung weight and changes in bronchoalveolar lavage parameters, as well as microscopic findings in the respiratory tract. The e-vapor groups had minimal microscopic changes, including squamous metaplasia in laryngeal epiglottis, and histiocytic infiltrates in the lung (Test-2 group only). The 3R4F group had a higher incidence and severity of microscopic findings compared to any e-vapor group. Transcriptomic analysis also showed that the 3R4F group had the highest number of differentially expressed genes compared to Sham Control. Among e-vapor groups, Test-2 group had more differentially expressed genes but the magnitude of gene expression-based network perturbations in all e-vapor groups was ∼94% less than the 3R4F group. On proteome analysis in the lung, differentially regulated proteins were detected in the 3R4F group only. In conclusion, 3-weeks of 3R4F exposure induced molecular and microscopic changes associated with smoking-related diseases in the respiratory tract, while e-vapor exposures showed substantially reduced biological activities.
2021-02-28 | E-MTAB-10166 | biostudies-arrayexpress
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:normal human bronchial epithelial cultures from two cultures in parallel exposed to cigarette smoke (CS) or air (mock) at timepoints 4 hours and 24 hours. Keywords = cigarette smoke Keywords = microarray Keywords = bronchial cell Keywords = tobacco Keywords: time-course
2005-02-23 | GSE2302 | 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:Kentucky assay: cigarette smoke
| PRJNA626542 | ENA
Project description:Liver represents one of the most important organs involved in the elimination of xenobiotic and potentially toxic substances. Cigarette smoke (CS) contains several compounds that exert biological effects and cause smoking related diseases. Although cigarette smoke is not directly hepatotoxic, a growing body of evidence suggests that CS may exacerbate chronic liver diseases. Here we integrated classical toxicological endpoints with molecular measurement and computational analysis approaches to investigate exposure effects on liver in an Apoe-/- mouse study. The mice were exposed to high concentrations of 3R4F reference CS (600 mg/m3 TPM, 29.9 mg/m3 nicotine), aerosol from a candidate modified risk tobacco product (MRTP), the Tobacco Heating System (THS) 2.2, or filtered air (Sham) for up to 8 months. After 2 months of CS exposure, some groups were either switched to the MRTP or underwent cessation. While clear signs of hepatotoxic effects were absent for any exposure group, the integrative analysis of proteomic and transcriptomic data showed a CS-dependent impairment of specific biological networks, such as lipid, xenobiotic, and iron homeostasis, which likely in turn mutually contribute to worsening of the oxidative stress. In contrast, most of these changes were absent in mice exposed to THS2.2, and in the cessation and in the switching groups. Our findings shed light on the complex biological response of the liver to CS exposure and support the benefits of switching to the tested heat-not-burn product, THS2.2.
2016-10-31 | E-MTAB-3876 | biostudies-arrayexpress