Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA125277 | ENA |
REPOSITORIES: ENA
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Project description:AAmiodarone is an antiarrhythmic drug and representatively induce pulmonary phospholipidosis. Amiodarone-induced toxicity has been a serious unpredictable side effect of the treatment and an important clinical problem. Possible causes include allergic, cytotoxic or immunologic reactions to this agent. We examined the consequences of the mechanism of amiodarone-induced pulmonary toxicity gene expression in BEAS-2B cells, huma bronchial cell line, by microarray. The expression of these genes are potential biomarker of amiodarone-induced pulmonary toxicity. Also, We provide a clue about mechanism of pulmonary toxic action by these clinical chemotherapeutic agents. BEAS-2B cells were seeded and after incubation for 24 h at 37C, the cells were treated with 29.388 μM(IC20) amiodarone for 48 h. And after total RNA isolation, gene expression analysis was conducted using a 44-k whole human genome microarray. Labeling and hybridization were performed using a FairPlay microarray labeling kit, followed by the coupling of Cy3 (controls) or Cy5 (treated samples) dye. The hybridized slides were scanned using a GenePix 4000B microarray scanner, and the images were analyzed using GenePix 4.1 software to obtain gene expression ratios. The fluorescence intensity of each spot was calculated by local median background subtraction. We then used the robust scatter-plot smoother LOWESS function to perform intensity-dependent normalization of gene expression. Scatter-plot analysis was performed using Microsoft Excel 2000. A significance analysis of microarray (SAM) was performed for genes with significant changes in expression.
2011-01-10 | E-GEOD-20582 | biostudies-arrayexpress
Project description:AAmiodarone is an antiarrhythmic drug and representatively induce pulmonary phospholipidosis. Amiodarone-induced toxicity has been a serious unpredictable side effect of the treatment and an important clinical problem. Possible causes include allergic, cytotoxic or immunologic reactions to this agent. We examined the consequences of the mechanism of amiodarone-induced pulmonary toxicity gene expression in BEAS-2B cells, huma bronchial cell line, by microarray. The expression of these genes are potential biomarker of amiodarone-induced pulmonary toxicity. Also, We provide a clue about mechanism of pulmonary toxic action by these clinical chemotherapeutic agents.
2011-01-10 | GSE20582 | GEO
Project description:MicroRNA levels in non-transformed BEAS-2B bronchial epithelial cells, two lines of mycoplasma transformed BEAS-2B cells, and A549 lung adenocarcinoma cells were measured. Microarray analyses of 1145 microRNAs in A549 lung adenocarcinoma cells and two other transformed lung cell types relative to BEAS-2B bronchial epithelial cells were performed. 106 miRNAs were down-regulated and 69 miRNAs were up-regulated in all three transformed lines
2014-03-11 | GSE55748 | GEO
Project description:Microarray Analysis of Differentially Expressed Genes in human bronchial cells(BEAS-2B) treated MTX
| PRJNA103769 | ENA
Project description:Total RNA samples from human bronchial epithelial BEAS-2B passage-matched control cells and Cr(VI)-transofmred BEAS-2B cells were submitted to ArraySatr for total RNA m6A epitranscriptomic microarray analysis
2022-06-29 | GSE186605 | GEO
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:Human bronchial epithelial cells (BEAS-2B cells) were treated with RSV at 1.0 MOI for 4 and 24 hours or control (vehicle-treated for 4 hours). Global gene expression was measured by Affy Hu133 plus 2.0 microarray chips. Keywords: Inflammation, microtubules, RSV, time course
2006-05-01 | GSE3397 | GEO
Project description:MicroRNA levels in non-transformed BEAS-2B bronchial epithelial cells, two lines of mycoplasma transformed BEAS-2B cells, and A549 lung adenocarcinoma cells were measured. Microarray analyses of 1145 microRNAs in A549 lung adenocarcinoma cells and two other transformed lung cell types relative to BEAS-2B bronchial epithelial cells were performed. 106 miRNAs were down-regulated and 69 miRNAs were up-regulated in all three transformed lines The control cells were the human non-transformed BEAS-2B cells (Lechner JF, LaVeck MA. A serum-free method for culturing normal human bronchial epithelial cells at clonal density. J. Tissue Culture Methods 9: 43-48, 1985). The BEAStra1 and BEAStra2 cells were replicate populations of BEAS-2B cells that were transformed following infection with mycoplasma (Jiang, S., Zhang, S., Langenfeld, J., Lo, S.C., and Rogers, M.B., Mycoplasma infection transforms normal lung cells and induces bone morphogenetic protein 2 expression by post-transcriptional mechanisms. J Cell Biochem. 104(2): 580-594, 2007). A459 lung adenocarcinoma cells were derived from a human lung tumor (Giard DJ, et al. In vitro cultivation of human tumors: establishment of cell lines derived from a series of solid tumors. J. Natl. Cancer Inst. 51: 1417-1423, 1973. PubMed: 4357758).
2014-03-11 | E-GEOD-55748 | 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-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:We reported the application of next generation sequencing technology for high-throughput profiling of miRNA expression in bronchile epithelial cell line Beas-2b with epithelial or mesenchymal mophology. By comparation the expression aboundence of known miRNAs between epithelial type and mesenchymal type Beas-2b cells, we found both upregulated and downregulated miRNAs in bronchial epithelial cells during EMT. This study provides a basic condition for further investigation of the roles of the regulated miRNAs during EMT in bronchial epithelial cells.
2018-12-26 | GSE117522 | GEO