Transcriptional response of Mycobacterium tuberculosis to cigarette smoke condensate
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA721867 | ENA |
REPOSITORIES: ENA
Similar Datasets
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:This SuperSeries is composed of the following subset Series:; GSE14383: Effects of chronic exposure of human bronchial epithelial cells to low doses of cigarette smoke condensate; GSE14385: Response of bronchial epithelial cells to low doses of cigarette smoke condensate and subsequent demethylation agent Experiment Overall Design: Refer to individual Series
2009-08-09 | E-GEOD-14461 | biostudies-arrayexpress
Project description:The study seeks to identify the epigenetic changes caused by exposure of to cigarette smoke condensate. To this goal human bronchial epithelial cells, BEAS-2B, were treated with 5-aza-2’deoxycitidine and trychostatin A (5AzaC/TSA) subsequent to a chronic exposure (1 month) to cigarette smoke condensate (CSC). As negative control served BEAS-2B cells that were untreated or treated with CSC/DMSO for one month without the subsequent application of 5Aza/TSA. Keywords: stress response
2009-08-01 | GSE14385 | GEO
Project description:Little is known about alteration of the global gene expression by cigarette smoke (CS) and few biomarkers for smoking-related harm are available. We used Affymetrix HG-U133A GeneChips to measure the transcriptomes in eight cultured lymphocyte samples exposed to cigarette smoke condensate (CSC) in vitro . The in vitro exposure of lymphocytes to CSC significantly changed expression levels of 2,266 genes many of which biologically interacted. They included genes encoding for xenobiotic metabolism and oxidative stress-response (e.g. Nrf2 and AhR signaling pathways), inflammation/immune response (e.g. cytokines), apoptosis, cell cycle and tumorigenesis. However, the magnitude of expression responses for some genes showed high inter-individual variability. Experiment Overall Design: The goals of this study were to evaluate novel gene expression profiles and pathways affected by cigarette smoke condensate (CSC), and to identify potential biomarkers for cigarette smoke exposure and harm. To this end, we isolated the PBMC from eight light smokers, cultured the cells in vitro and exposed them to 2R4F CSC, then determined the gene expression profiles with Affymetrix microarray and analyzed alteration of global gene expression after exposure to CSC.
2009-09-15 | E-GEOD-12586 | biostudies-arrayexpress
Project description:Cigarette smoke is a risk factor for inflammatory diseases, such as atherosclerosis. Tobacco smoke interacts with inflammatory cytokines to produce endothelial dysfunction and induces pro-inflammatory and pro-atherosclerotic effects in vascular tissue. Smooth muscle cells (SMCs) are present in the media of human arteries, and are considered protective against atherosclerotic plaque destabilization. Contractile SMCs are the most prominent cell type in the healthy vessel wall. SMCs are not terminally differentiated, and retain the ability to undergo a phenotypic switch from a contractile to a dedifferentiated synthetic state to express inflammatory markers and a phagocytic activity in response to environmental cues. The aim of our study was to evaluate the effects in human SMCs of lipophilic component from cigarette smoke condensate (CSC) and of hydrophilic components of Electronic-cigarette, Tobacco heating products, or cigarette smoke.
2023-05-10 | PXD041174 | Pride
Project description:The study seeks to identify the epigenetic changes caused by exposure of to cigarette smoke condensate. To this goal human bronchial epithelial cells, BEAS-2B, were treated with 5-aza-2âdeoxycitidine and trychostatin A (5AzaC/TSA) subsequent to a chronic exposure (1 month) to cigarette smoke condensate (CSC). As negative control served BEAS-2B cells that were untreated or treated with CSC/DMSO for one month without the subsequent application of 5Aza/TSA. Experiment Overall Design: BEAS-2B Cells were treated for one month with CSC, DMSO, and left untreated. Subsequently half of the samples were treated with the demethylation agent. So that there were six different conditions with three biological replicates each. One sample had to be excluded because of low quality.
2009-08-15 | E-GEOD-14385 | biostudies-arrayexpress
Project description:Little is known about alteration of the global gene expression by cigarette smoke (CS) and few biomarkers for smoking-related harm are available. We used Affymetrix HG-U133A GeneChips to measure the transcriptomes in eight cultured lymphocyte samples exposed to cigarette smoke condensate (CSC) in vitro . The in vitro exposure of lymphocytes to CSC significantly changed expression levels of 2,266 genes many of which biologically interacted. They included genes encoding for xenobiotic metabolism and oxidative stress-response (e.g. Nrf2 and AhR signaling pathways), inflammation/immune response (e.g. cytokines), apoptosis, cell cycle and tumorigenesis. However, the magnitude of expression responses for some genes showed high inter-individual variability. Keywords: toxic effects on gene expression
2009-08-28 | GSE12586 | GEO
Project description:Exposure to genotoxic stresses such as cosmic radiation and second-hand tobacco smoke may increase the risk of breast cancer formation. Towards an understanding of how exposure to these genotoxic agents affect breast cancer biogenesis, we have shown that treating non-tumorigenic immortalized breast MCF 10A cells with low doses (0.1 Gray) of radiation as well as cigarette smoke condensate can generate a neoplastic breast cancer phenotype. The transformed phenotype promoted increased mammosphere numbers, altered cell cycle phases, and increased invasion and motility. In addition, exclusion of Hoechst 33342 dye, a surrogate marker for increased ABC transporters, was observed, which indicates a possible increase in drug resistance. Furthermore, differential gene expression profiles were generated from the individual and combination treatment. Overall, the results indicate that when normal breast cells are exposed to low dose radiation in combination with cigarette smoke condensate a phenotype is generated that exhibits traits indicative of neoplastic transformation. Taken together, these results provide a new insight into a possible etiology for breast cancer formation in individuals exposed to cosmic radiation and second-hand smoke. To study the effects of low dose ionizing radiation and tobacco smoke on breast cells, MCF 10A cells were treated either with radiation (Rad - 0.1 Gray) or cigarette smoke condensate (Csc - 10 microgram/ml of medium) or a combination of Rad + Csc). Following treatments, the cells were incubated for 72 hr, RNA extracted and analyzed for differential gene expression pattern.
2010-07-07 | E-GEOD-21066 | biostudies-arrayexpress
Project description:Exposure to genotoxic stresses such as cosmic radiation and second-hand tobacco smoke may increase the risk of breast cancer formation. Towards an understanding of how exposure to these genotoxic agents affect breast cancer biogenesis, we have shown that treating non-tumorigenic immortalized breast MCF 10A cells with low doses (0.1 Gray) of radiation as well as cigarette smoke condensate can generate a neoplastic breast cancer phenotype. The transformed phenotype promoted increased mammosphere numbers, altered cell cycle phases, and increased invasion and motility. In addition, exclusion of Hoechst 33342 dye, a surrogate marker for increased ABC transporters, was observed, which indicates a possible increase in drug resistance. Furthermore, differential gene expression profiles were generated from the individual and combination treatment. Overall, the results indicate that when normal breast cells are exposed to low dose radiation in combination with cigarette smoke condensate a phenotype is generated that exhibits traits indicative of neoplastic transformation. Taken together, these results provide a new insight into a possible etiology for breast cancer formation in individuals exposed to cosmic radiation and second-hand smoke.
2010-06-21 | GSE21066 | GEO
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.
2022-03-02 | PXD007108 | Pride