Transcriptional profiling of human bronchial epithelial cell BEAS-2B exposed to diesel and biomass ultrafine particles
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ABSTRACT: Time course transcriptomic profiling of human bronchial epithelial cell BEAS-2B exposed to a single dose of diesel and biomass ultrafine particles
Project description:Airway smooth muscle cells were stimulated with conditioned medium from BEAS-2B cells in the absence (Control) or Inhibition of miR-210.
Project description:To explore the host responses associated with TLR3 signaling during IAV infection, we used a human bronchial epithelial cell line stably expressing a dominant negative form of TLR3 (pZERO-hTLR3) and examined global impact of TLR3 through an analysis of gene expression changes compared to control cells at 24 h after infection.
Project description:GS-5759 is a bifunctional ligand composed of a quinolinone-containing pharmacophore found in several β2-adrenoceptor agonists linked covalently to a phosphodiesterase 4 inhibitor (PDE4) related to GSK 256066 by a pent-1-yn-1-ylbenzene spacer. The object of the study was to detemine if gene expression changes induced by GS-5759 were replicated by a β2-adrenoceptor agonist (indacaterol; Ind) and a PDE4 inhibitor (GSK 256066; GSK) in combination. Microarray analysis was performed on RNA from BEAS-2B cells treated with GS-5759 and a combination of indacaterol and GSK 256066 to identify differentialy expressed genes. Confluent BEAS-2B cells were treated with vehicle, Ind/GSK or GS-5759 for 1h, 2h, 6h or 18h. Total RNA was extracted, quantified (NanoDrop 2000) and the quality of each sample determined by using the Agilent 2100 Lab-on-a-Chip system before being processed for gene expression chnages by Expression Analysis Inc (Dunham, NC, USA).
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
Project description:In the present study, we discovered an unexpected interplay between immunometabolism and antiviral immunity. Profiling of human bronchial epithelial BEAS-2B cells was performed using Agilent’s SurePrint G3 human gene expression microarray kit. A single-color design provided two types of comparison: (i) IAV-infected versus mock-infected cells, and (ii) succinate-treated infected cells versus mock-infected cells.
Project description:Alterations in chromatin modifications, including DNA methylation and histone modification patterns, have been characterized under exposure of several environmental pollutants, including nickel. As with other carcinogenic metals, the mutagenic potential of nickel compounds is low and is not well correlated with its carcinogenic effects. Nickel exposure, however, is associated with alterations in chromatin modifications and related transcriptional programs, suggesting an alternative pathway whereby nickel exposure can lead to disease. To investigate the extent to which nickel exposure disrupts chromatin patterns, we profiled several histone modifications, including H3K4me3, H3K9ac, H3K27me3 and H3K9me2 as well as the insulator binding protein CTCF and the transcriptomes of control BEAS-2B cells and cells treated with nickel for 72 hours. Our results show significant alterations of the repressive histone modification H3K9me2 in nickel-exposed cells with spreading of H3K9me2 into new domains associated with gene silencing. We furthermore show that local regions of active chromatin can protect genes from nickel-induced H3K9me2 spreading. Interestingly, we show that nickel exposure selectively disrupts weaker CTCF sites, leading to spreading of H3K9me2 at these regions. These results have major implications in the understanding of how environmental carcinogens can affect chromatin dynamics and the consequences of chromatin domain disruption in disease progression. Treat BEAS-2B cells with NiCl2 for 72 hours and compare histone modification, CTCF binding to control BEAS-2B cells to see how they regulated gene expression by RNA-seq
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.
Project description:BEAS-2B cells have been treated with low doses (20 ug/ml) of CSC for 4 months. As negative control BEAS-2B cells were treated with DMSO (the CSC solvent). Non-treated cells were cultivated in parallel. Experiment Overall Design: After each month total RNA was extracted from three replicates of CSC, DMSO and non-treated BEAS-2B cells and hybridized to Affymetrix GeneChips.
Project description:This work details the first global mass spectrometric analysis of histone H2B variants as cells undergo arsenic-mediated epithelial to mesenchymal transition.
Project description:Human bronchial lung cells (BEAS-2B) were treated for 6 weeks with low doses (1 µg/mL) of Ag nanoparticles (10 nm citrate coated). At the end of the exposure control and treated samples were submitted for RNA-Seq analysis (Hiseq2500). The overall goal of this experiment was to gain an in-depth understanding of the transcriptomic changes induced by low-dose, long-term exposure of human lung cells to Ag nanoparticles and to generate hypotheses related to their mechanisms of toxicity.