Frontal Cortex Transcriptome Analysis of Mice Exposed to Electronic Cigarettes During Early Life Stages
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE75858 | GEO | 2016/02/01
SECONDARY ACCESSION(S): PRJNA305535
REPOSITORIES: GEO
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Project description:Our study demonstrated that e-cigarettes, both with and without nicotine, induced sex-dependent gene expression change. This RNA-seq study examined the expression profiles of brain frontal cortex samples from mice exposed to classic tobacco flavored blu⢠e-cigarettes during gestation and lactation. Brains were extracted and sectioned from ~1-month-old male and female offspring the week following exposure, RNA was isolated and purified from frontal cotrex tissues, and gene expression profiles were analyzed by RNA Sequencing.
2016-02-01 | E-GEOD-75858 | biostudies-arrayexpress
Project description:We previously put forward a multi-layer systems toxicology framework for in vitro assessment of e-liquids that is meant to complement the battery of classical assays for genotoxicity testing. The framework started with the first layer to screen e-liquids for their potential toxicity, followed by the second layer to investigate the toxicity-related mechanism of a selected e-liquid(s), and finally the third layer to evaluate the toxicity-related mechanism of the corresponding aerosol(s). In this work, we leveraged this framework to assess the biological impact of an e-liquid MESH™ “Classic Tobacco” and its aerosol in comparison with the impact of 3R4F reference cigarettes. In the first layer, we evaluated the cytotoxicity profile of the MESH Classic Tobacco liquid (containing humectants, nicotine, and flavors) and its Base liquid (containing humectant and nicotine only) in comparison with total particulate matter (TPM) of 3R4F cigarette smoke (CS). In the second layer, we explored changes in specific markers using high content screening assays to identify potential toxicity-related mechanisms of the MESH Classic Tobacco and Base liquids beyond cell viability compared with the 3R4F TPM-induced effects. In the third layer, we compared the biological impact of exposure to the MESH Classic Tobacco aerosol with CS using human organotypic buccal and small airway epithelial cultures. The results showed that the cytotoxicity profile of the MESH Classic Tobacco liquid was similar to the Base liquid but lower than the toxicity of 3R4F TPM at comparable nicotine concentrations. When compared with CS exposure, MESH Classic Tobacco aerosol exposure did not cause tissue damage and elicited lower changes in the global mRNA, global microRNA, and protein markers. The global mRNA changes following Classic Tobacco aerosol exposure indicated perturbations in processes related to cell fate, cell stress, and inflammatory response that were less than 20% of the perturbations following CS exposure. In the context of tobacco-harm reduction strategy, the framework is suitable to assess the potential reduced impact of EC aerosol relative to CS.
2019-11-01 | E-MTAB-7912 | biostudies-arrayexpress
Project description:We previously put forward a multi-layer systems toxicology framework for in vitro assessment of e-liquids that is meant to complement the battery of classical assays for genotoxicity testing. The framework started with the first layer to screen e-liquids for their potential toxicity, followed by the second layer to investigate the toxicity-related mechanism of a selected e-liquid(s), and finally the third layer to evaluate the toxicity-related mechanism of the corresponding aerosol(s). In this work, we leveraged this framework to assess the biological impact of an e-liquid MESH™ “Classic Tobacco” and its aerosol in comparison with the impact of 3R4F reference cigarettes. In the first layer, we evaluated the cytotoxicity profile of the MESH Classic Tobacco liquid (containing humectants, nicotine, and flavors) and its Base liquid (containing humectant and nicotine only) in comparison with total particulate matter (TPM) of 3R4F cigarette smoke (CS). In the second layer, we explored changes in specific markers using high content screening assays to identify potential toxicity-related mechanisms of the MESH Classic Tobacco and Base liquids beyond cell viability compared with the 3R4F TPM-induced effects. In the third layer, we compared the biological impact of exposure to the MESH Classic Tobacco aerosol with CS using human organotypic buccal and small airway epithelial cultures. The results showed that the cytotoxicity profile of the MESH Classic Tobacco liquid was similar to the Base liquid but lower than the toxicity of 3R4F TPM at comparable nicotine concentrations. When compared with CS exposure, MESH Classic Tobacco aerosol exposure did not cause tissue damage and elicited lower changes in the global mRNA, global microRNA, and protein markers. The global mRNA changes following Classic Tobacco aerosol exposure indicated perturbations in processes related to cell fate, cell stress, and inflammatory response that were less than 20% of the perturbations following CS exposure. In the context of tobacco-harm reduction strategy, the framework is suitable to assess the potential reduced impact of EC aerosol relative to CS.
2019-11-01 | E-MTAB-7911 | biostudies-arrayexpress
Project description:Analysis of primary human bronchial epithelial cells grown in air liquid interface, exposed in vitro to whole tobacco cigarette smoke (48 puffs, 48 minutes) and electronic cigarette aerosol (400 puffs, 200 minutes). Electronic cigarette exposures included two flavors (menthol, tobacco) both with, and without nicotine.
2016-10-12 | GSE82137 | GEO
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:Electronic cigarettes (e-cigarettes) have gained their popularity as a substitute for cigarettes or cigars. Despite the widespread use of flavoring chemicals in e-cigarettes, the health impacts of the flavoring compounds, in particular their effects on critical cellular function in the lung, remain largely unknown. The goal of this study was to identify transcriptomic changes and impacted biological pathways in primary human bronchial epithelial cells (HBECs) exposed to flavoring chemicals (diacetyl or 2,3-pentanedione) and to flavored e-cigarette smoke. An airway-liquid interface culturing method was used to differentiate primary human bronchial epithelial cells (HBECs) into mature epithelial cells, which were then treated with 25 ppm diacetyl, 100 ppm 2,3 pentanedione, or e-cigarette smoke solution containing 2 ppm diacetyl. Poly(A)-selected RNA-Seq libraries were prepared with the PrepX RNA-Seq for Illumina Library kit. An Illumina HiSeq 2500 instrument was used to generate 50 base pair single-end reads. STAR was used to align sequencing reads to the hg38 reference genome, and HTSeq was used to quantify transcript levels. DESeq2 was used to perform differential expression analysis.
2019-08-21 | GSE118431 | GEO
Project description:Electronic cigarette (EC) use has grown substantially since entry into the US market, particularly among adolescents and combustible tobacco users. Despite growing popularity and claims of harm reduction, the health effects of these products outside the lung is poorly understood. Several constituents of cigarette smoke (CS) with known neurovascular and inflammatory effects are present in EC liquids or formed during the generation of vapor. The present study characterizes the impact of EC exposure on neuroinflammation and blood-brain barrier (BBB) function, and provides comparison of outcomes with reference cigarette exposure normalized to comparable levels of nicotine delivery. Additionally, the contribution of nicotine to observed effects is elucidated through comparison with EC liquids which are verified to be nicotine-free. C57BL/6 mice are exposed to 2 hrs of daily EC vapor or CS, beginning at 8 wks of age. Changes in BBB gene expression are first characterized by whole exome sequencing of isolated brain microvessels following chronic (2 month) EC exposure.
2020-11-23 | GSE142400 | GEO
Project description:Combustible cigarettes produce many toxic substances that have been linked to diseases such as lung cancer and chronic obstructive pulmonary disease (COPD). Electronic cigarettes (e-cigarettes) can be used as an alternative to cigarettes for smokers who are unable or unwilling to quit. However, the effects and mechanisms of e-cigarette aerosol (ECA) on respiratory function have not been fully elucidated, and in vivo studies of its safety are limited compared to cigarette smoke (CS). In this article, we chose nicotine levels as the dose reference and selected C57BL/6 mice for a 10-week subchronic inhalation toxicity study. A comprehensive set of toxicological endpoints was used to study the effects of exposure. Thus, additional evidence is provided for the relative safety of e-cigarettes.
2022-07-14 | PXD035374 | iProX
Project description:Exposure to secondhand tobacco smoke during early childhood has been linked with an increased risk for behavioral disorders, yet little is known regarding how brain development is impacted. Using an environmental tobacco smoke (ETS) passive inhalation model, this study assesses the neurodevelopmental impact of juvenile exposure during a critical period of frontal cortex development, specifically that of the rat orbital neocortex between postnatal days 8 and 22. Agnostic shotgun proteomics was employed to discern the biomolecular shift within this rapidly developing brain region that is responsible for higher-order behavioral control. The orbital cortex neuroproteome was assessed between ETS-exposed and room-air control animals employing a label-free shotgun approach with data-independent acquisition. Following protein roll-up, a total of X protein were found statistically altered in quantity out of Y total proteins identified. These results implicate a prominent shift within metabolic processes and synaptic organization related to excitatory and inhibitory neurotransmission. Findings derived from this dataset may further our understanding of how secondhand smoke exposure can perturb the orbital frontal cortex and result in developmental behavioral disorders.
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