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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: wenyue sun

PROVIDER: E-GEOD-24414 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Chronic CSE treatment induces the growth of normal oral keratinocytes via PDK2 upregulation, increased glycolysis and HIF1α stabilization.

Sun Wenyue W Chang Steven S SS Fu Yumei Y Liu Yan Y Califano Joseph A JA

PloS one 20110119 1

<h4>Background</h4>Exposure to cigarette smoke is a major risk factor for head and neck squamous cell carcinoma (HNSCC). We have previously established a chronic cigarette smoke extract (CSE)-treated human oral normal keratinocyte model, demonstrating an elevated frequency of mitochondrial mutations in CSE treated cells. Using this model we further characterized the mechanism by which chronic CSE treatment induces increased cellular proliferation.<h4>Methodology/principal findings</h4>We demonst ...[more]

PMID: 21283817

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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.

2011-02-10 | GSE24414 | 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

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

Oxidative stress induces mitochondrial dysfunction and a protective unfolded protein response in RPE cells

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2014-01-30 | E-GEOD-49107 | biostudies-arrayexpress

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

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2011-08-30 | E-GEOD-30660 | biostudies-arrayexpress

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 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

Proteomic analysis of vocal fold fibroblasts exposed to cigarette smoke extract

Project description:Reinke’s edema is a cigarette associated, benign, mostly bilateral lesion of the vocal folds leading to dysphonia and dyspnea. Until today information about pathophysiology is only scarce, treatment is only surgical. To explore the pathophysiology of Reinke’s edema, we exposed near primary human vocal fold fibroblasts to cigarette smoke extract enriched medium or air bubbled control for 24 hrs. followed by a proteomic analysis. Proteomic analyses revealed an increase of proteins involved in oxidative stress response. We furthermore found that a significant number of essential extracellular matrix proteins was altered by culturing human VFF with CSE enriched medium: UDP-glucose 6-dehydrogenase, a protein involved in hyaluronan synthesis was upregulated, while the expression of several fibrillar collagen types was significantly reduced. The current findings corroborate previous studies but revealed new insights in possible disease mechanisms of Reinke’s edema too. We postulate that changes in the composition -reduction of collagen fibrils, increase of hyaluronan- of the vocal folds’ ECM may lead to the clinical findings.

2019-08-06 | PXD010640 | Pride

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