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Human primary alveolar epithelial cells (hAEC) exposed to cigarette smoke extract

ABSTRACT: Human primary alveolar epithelial cells (hAEC) exposed to cigarette smoke extract

PROVIDER: PRJNA773500 | ENA |

REPOSITORIES: ENA

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Human primary alveolar epithelial cells (hAEC) exposed to cigarette smoke extract

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.

2021-10-28 | GSE186359 | GEO

Human alveolar epithelial cells (A549) exposed to cigarette smoke extract

2016-02-16 | GSE77942 | GEO

Human alveolar epithelial cells (A549) exposed to cigarette smoke extract

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. Human alveolar epithelial cells stimulated with three different concentractions of CSE (1%, 5% and 10%) and for 1, 3 and 5 weeks were used for RNA extraction and hybridization on Affymetrix microarrays.

2016-02-16 | E-GEOD-77942 | biostudies-arrayexpress

Cigarette smoke extract-treated alveolar macrophage-derived extracellular vesicles

Project description:This project is based upon the fundamental observation that alveolar macrophage-derived extracellular vesicles (AM-EVs), when internalized by neighboring epithelial cells, inhibit their infection by influenza virus. This inhibitory activity of AM-EVs is abolished when AMs are treated with cigarette smoke extract (CSE). We chose to survey the AM-EV proteome in an effort to identify candidate proteins whose abundance within EVs was downregulated by CSE treatment of AMs, thus explaining the ability of CSE to abrogate the inhibitory activity against influenza.

2020-06-09 | PXD019528 | Pride

Mitochondrial mutations in cigarette smoke extract-chronically treated human oral OKF6 cells

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Temporal transcriptional response of endothelial cells to aqueous cigarette smoke extract exposure

Project description:Endothelial cells (HUVEC) were exposed to cigarette smoke extract for 3, 7, and 24 hours. Total RNA was isolated and used for hybridisation to dual channel oligonucleotide genome-wide microarrays using untreated HUVEC as a control. The objective was to find out what genes are regulated by exposure to cigarette smoke extract, and the time dependency of their regulation Keywords: time course, stress response

2007-01-26 | GSE6854 | GEO

Mitochondrial mutations in cigarette smoke extract-chronically treated human oral OKF6 cells

Project description:The objective of this study was to analyze the mitochondrial mutations induced by chronic cigarette smoke extract treatment in human oral immortal OKF6 cells. The objective of this study was to analyze the mitochondrial mutations induced by chronic cigarette smoke extract treatment in human oral immortal OKF6 cells. 2 samples were included, a control passaged human oral immortal OKF6 cells and cigarette smoke extract-treated OKF6 cells. The chronic treatment for cigarette smoke extract is 7 months. Genomic DNAs were extracted from both cells and then used for Affymetix MitoChip Version 2.0 analysis.

2011-02-10 | E-GEOD-24414 | biostudies-arrayexpress

Human airway epithelial responses to rhinovirus infection and cigarette smoke extract alone and in combination

Project description:This study was performed to test the hypothesis that cigarette smoke extract would alter the responses of primary cultures of human bronchial epithelial cells to infection with purified human rhinovirus 16. The data show marked alterations in rhinovirus-induced expression profiles of a number of genes in the presence of cigarette smoke extract (CSE).

2011-03-15 | GSE27973 | GEO

A549 cigarette smoke resistant cell line expression profiling

Project description:Chronic obstructive pulmonary disease (COPD) is currently the third cause of death worldwide with still increasing mortality and morbidity. Primary etiology of COPD is cigarette smoking. However, in clinic, not all smokers develop COPD. The underlying mechanism remains unclear. A549 cells, which are widely used in vitro as a model of alveolar type II pulmonary epithelium, were subjected to step-wise increasing cigarette smoke extract (CSE) treatments. Those cigarette smoke extract resistant (SER) cells were cultured and used for further experiments. The aim of this study is to investigate the differentially expressed genes in SER group with or without CSE treatment and identify potential genes or pathways which could play a role in COPD pathogenesis.

2024-01-01 | GSE222965 | GEO

Cigarette smoke alters the secretome of lung epithelial cells

Project description:Cigarette smoke is the most relevant risk factor for the development of lung cancer and chronic obstructive pulmonary disease. Many of its more than 4500 chemicals are highly reactive, thereby altering protein structure and function. Here, we used subcellular fractionation coupled to label-free quantitative MS to globally assess alterations in the proteome of different compartments of lung epithelial cells upon exposure to cigarette smoke extract. Proteomic profiling of the human alveolar derived cell line A549 revealed the most pronounced changes within the cellular secretome with preferential downregulation of proteins involved in wound healing and extracellular matrix organization. In particular, secretion of secreted protein acidic and rich in cysteine, a matricellular protein that functions in tissue response to injury, was consistently diminished by cigarette smoke extract in various pulmonary epithelial cell lines and primary cells of human and mouse origin as well as in mouse ex vivo lung tissue cultures. Our study reveals a previously unrecognized acute response of lung epithelial cells to cigarette smoke that includes altered secretion of proteins involved in extracellular matrix organization and wound healing. This may contribute to sustained alterations in tissue remodeling as observed in lung cancer and chronic obstructive pulmonary disease.

2019-01-08 | PXD007180 | Pride

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