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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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The Effect of Repeated Whole Cigarette Smoke Challenge on Human Air-Liquid Interface Lung Epithelial Cultures

ABSTRACT: Airway epithelial cells are the first cells of the lungs to be exposed to the toxic agents contained within cigarette smoke. Accordingly, the response of these cells to this challenge is of considerable interest in the context of diseases in which cigarette smoke is a major aetiological factor. We used Affymetrix microarrays to study the effects of repeated cigarette smoke challenge on three-dimensional human lung airway epithelial cultures. We have used cultures from four individual donors, and compared the effects of repeated cigarette smoke challenge (30mins exposure on four separate days), with no challenge.

ORGANISM(S): Homo sapiens

SUBMITTER: Iain Dougall

PROVIDER: E-GEOD-30660 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The Effect of Repeated Whole Cigarette Smoke Challenge on Human Air-Liquid Interface Lung Epithelial Cultures

Project description:Airway epithelial cells are the first cells of the lungs to be exposed to the toxic agents contained within cigarette smoke. Accordingly, the response of these cells to this challenge is of considerable interest in the context of diseases in which cigarette smoke is a major aetiological factor. We used Affymetrix microarrays to study the effects of repeated cigarette smoke challenge on three-dimensional human lung airway epithelial cultures.

2011-08-31 | GSE30660 | GEO

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2020-03-31 | E-MTAB-8155 | biostudies-arrayexpress

Transcription profiling of rat tracheal airway explant treated with cigarette smoke.

Project description:Although a number of animal model studies have addressed changes in gene expression in the parenchyma and their relationship to emphysema, much less is known about the pathogenesis of cigarette smoke-induced small airway remodeling. In this study we exposed rat tracheal explants to whole smoke for 15 minutes, and then cultured the explants in air. The airway transcriptome was evaluated using RAE 230_2 gene chips. By 2 hours after starting smoke exposure, expression levels of 502 genes were changed up or down by more than 1.5 times (p values <0.01 or less) and by 24 hours 1870 genes were significantly changed up or down. These included genes involved in anti-oxidant protection, epithelial defense and remodeling, inflammatory mediators and transcription factors, and a number of unexpected genes including the MMP-12 inducer, tachykinin-1 (substance P). Pre-treatment of the explants with 1 x 10-7 M dexamethasone reduced the number of significantly changed genes by approximately 47% at 2 hr and 68% at 24 hours and in almost all instances reduced the magnitude of the smoke-induced changes. We conclude that even a very brief exposure to cigarette smoke can lead to rapid changes in the expression of a large number of genes in rat tracheal explants, and that these effects are directly mediated by smoke, without a need for exogenous inflammatory cells. Steroids, contrary to the usual belief, are able to ameliorate many of these changes, at least in this very acute model. Experiment Overall Design: 4x tracheal explants (approx 2-3ug) from each rat (n=6 rats) exposed to control (air), smoke (10 puffs of cigarette smoke, delivered during 15 mins), dexamethasone and dexamethasone + cigarette smoke were used for RNA extraction and hybridization on Rat230_2 Affymetrix microarrays. 1 rat, 4 explants and 4 condiditons. n= 6 rats per group/condition 12 animals = 48 samples total (47 went into analysis because 1 sample failing QC metrics)

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Transcription profiling by array to investigate effect of repeated cigarette exposure on three-dimensional human bronchial epithelial cultures

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Gene expression data on lungs of wild-type and Rora (Retinoic acid related orphan receptor) mutant mice exposed to room air and smoke

Project description:Gene expression data on wild-type and Rora mutant mice exposed to room air and smoke. The results provide a general insight into the relationship of Rora to known DNA damage response pathways and its role in cigarette smoke-induced airspace enlargement. This dataset includes 4 wild-type mice exposed to room air, 4 wild-type mice exposed to cigarette smoke and 4 Rora mutant mice exposed to cigarette smoke.

2012-07-22 | E-GEOD-33512 | biostudies-arrayexpress

Cigarette smoke induces mitochondrial metabolic reprogramming in lung cells

Project description:Cigarette smoking remains the leading cause of non-small cell lung carcinoma. Studies involving acute exposure of smoke on lung cells revealed induction of pre- cancerous state in lung cells. Recently few studies have reported the chronic effect of cigarette smoke in inducing cellular transformation. Yet no systemic study has been performed to understand the molecular alterations in lung cells due to cigarette smoke. Hence it is both important and necessary to study the chronic effect of cigarette smoke in a temporal setting to understand the molecular alterations. In this study, we carried out TMT based proteomic profiling of lung cells which were exposed to cigarette smoke condensate (CSC) for upto 12 months. We identified 2621 proteins in total, of which 145, 114, 87, 169 and 671 proteins were differentially expressed (p<0.05, 1.5 fold) in 2nd, 4th, 6th, 8th and 12th month respectively. Pathway analysis revealed enrichment of xenobiotic metabolism signaling for the first 8 months of smoke treatment, where as continued exposure of smoke for 12 months revealed mitochondrial reprogramming in cells which includes dysregulation of oxidative phosphorylation machinery leading to enhanced reactive oxygen species and higher expression of enzymes involved in tricarboxylic acid cycle (TCA). In addition, chronic exposure of smoke led to overexpression of enzymes involved in glutamine metabolism, fatty acid degradation and lactate synthesis. This could possibly explain the availability of alternative source of carbon in TCA cycle apart from glycolytic pyruvate. Our data indicates that chronic exposure to cigarette smoke induces mitochondrial metabolic transformation in cells to support growth and survival.

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Organotypic human bronchial epithelial cultures (MucilAir) exposed to mainstream aerosols from the 3R4F cigarette and a novel tobacco vapor product

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

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Project description:Cigarette smoke has been associated with the development of various lung diseases including cancer. Dysregulation of miRNAs is known to affect protein expression which leads to diverse functional consequences. Investigating miRNA and protein expression in response to cigarette smoke exposure can lead to the identification of potential therapeutic and chemopreventive targets. We employed a SILAC-based quantitative proteomic analysis to identify proteins differentially expressed in response to cigarette smoke in H292 lung cancer cells. LC-MS/MS analysis led to the identification of 3,959 proteins, of which, 303 proteins were overexpressed and 112 proteins were found to be downregulated in cigarette smoke-treated H292 cells.

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