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: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
Project description:Repeated exposure and switching study of cigarette smoke and next generation tobacco product using 3D human bronchial epithelial cells
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:We investigated proteins identified by shotgun proteomics in cytologically normal airway epithelial cells from individuals at different levels of risk for lung cancer. We identified 2869 proteins in bronchial brushings from individuals at low, moderate or high risk for lung cancer. Pathway analysis revealed enrichment of carbohydrate metabolic pathways in high risk individuals. Differential expression of selected proteins was validated by parallel reaction monitoring mass spectrometry in separate individual bronchial brushings. Augmentation of glucose consumption and lactate production measured in human bronchial epithelial cell BEAS2B treated with cigarette smoke condensate and increased synthetic ability and reductive carboxylation revealed by metabolic flux analysis indicated profound metabolic reprogramming.