Project description:The aim of the present study was to characterize a common and unique signalling pathways associated to two seasonal particulate matter (PM) (winter PM2.5 and summer PM10) in human bronchial BEAS-2B cells by mean of a global transcriptomic profiling (including genes and miRNA) and the investigation of selected pathways at protein level.
Project description:The aim of the present study was to characterize a common and unique signalling pathways associated to two seasonal particulate matter (PM) (winter PM2.5 and summer PM10) in human bronchial BEAS-2B cells by mean of a global transcriptomic profiling (including genes and miRNA) and the investigation of selected pathways at protein level.
Project description:Bronchial epithelial cells represent the first line of defense against invading airborne pathogens. They are important contributors to innate mucosal immunity and provide a variety of anti-microbial effectors. To investigate the role of epithelial cells upon infection of airway pathogens, we stimulated BEAS-2B cells for 4 h with UV-inactivated bronchial pathogens including Staphylococcus aureus, Pseudomonas aeruginosa and Respiratory Syncitial Virus (RSV) that among other receptors can strongly activate TLR2, TLR4 and TLR3, respectively. Experiment Overall Design: All conditions were done in triplicates except for Staphylococcus aureus, were two replicates were done. As a control, unstimulated BEAS-2B were used. Altogether 11 arrays were hybridized.
Project description:Bronchial epithelial cells represent the first line of defense against invading airborne pathogens. They are important contributors to innate mucosal immunity and provide a variety of anti-microbial effectors. To investigate the role of epithelial cells upon infection of airway pathogens, we stimulated BEAS-2B cells for 4 h with UV-inactivated bronchial pathogens including Staphylococcus aureus, Pseudomonas aeruginosa and Respiratory Syncitial Virus (RSV) that among other receptors can strongly activate TLR2, TLR4 and TLR3, respectively. Keywords: expression profiling, response to pathogens
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
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
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.
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).
Project description:Time course transcriptomic profiling of human bronchial epithelial cell BEAS-2B exposed to a single dose of diesel and biomass ultrafine particles
