A549 cigarette smoke resistant cell line expression profiling
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ABSTRACT:
PROVIDER: PRJNA924293 | ENA |
REPOSITORIES: ENA
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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
Project description:We have investigated the effects of cigarette smoke exposure in three different strains of mice. DBA/2 and C57Bl/6J are susceptible to smoke and develop different lung changes in response to chronic exposure, while ICR mice are resistant to smoke and do not develop emphysema. The present study was carried out to determine early changes in the gene expression profile of mice exposed to cigarette smoke with either a susceptible or resistant phenotype.
2008-07-10 | GSE12036 | GEO
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
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.
2016-02-16 | GSE77942 | GEO
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:Kentucky assay: cigarette smoke
| PRJNA626542 | ENA
Project description:We have investigated the effects of cigarette smoke exposure in three different strains of mice. DBA/2 and C57Bl/6J are susceptible to smoke and develop different lung changes in response to chronic exposure, while ICR mice are resistant to smoke and do not develop emphysema. The present study was carried out to determine early changes in the gene expression profile of mice exposed to cigarette smoke with either a susceptible or resistant phenotype. Experiment Overall Design: Three strains of mice were exposed to smoke from three cigarette/day, 5d/wk for 4 weeks. Microarray analysis was carried out on total RNA extracted from the lung utilizing the Affymetrix platform.
2008-10-21 | E-GEOD-12036 | biostudies-arrayexpress
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
Project description:Mycbacterium tuberculosis was exposed to cigarette smoke condensate (CSC) in 7H9 dextrose culture media. The transcriptional response to cigarette smoke condensate was compared to that of exposure to the CSC diluent, DMSO..
2021-04-15 | GSE172041 | GEO
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