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
Project description:A variety of airborne pathogens can induce inflammatory responses in airway epithelial cells, which is a crucial component of host defence. However, excessive inflammatory responses and chronic inflammation also contribute to different diseases in the respiratory system. We hypothesized that the activation of protein kinase C (PKC) is one of the essential mechanisms of inflammatory responses in airway epithelial cells. In the present study, we stimulated human bronchial lung epithelial (BEAS-2B) cells with phorbol ester Phorbol 12, 13-dibutyrate (PDBu), and examined gene expression profile with microarray analysis. Bioinformatics suggested that PKC activation induced dramatic changes in gene expression related to multiple cellular functions. The top two functional networks of genes were centered on NFM-NM-:B and TNF-M-NM-1, which are two commonly known pathways for cell death and inflammation. Subsequent tests confirmed the decrease in cell viability and increase in the production of various cytokines. Interestingly, each of the increased cytokines was differentially regulated at mRNA and/or protein levels by different sub-class of PKC isozymes. We conclude that many pathogen-induced cell death and cytokine production in airway epithelial cells may be mediated through PKC related signaling pathways. These findings suggest that PKCs can be new targets for treatments of lung diseases. Three groups of BEAS-2B cells were prepared: control, 0.5 hour of PDBu stimulation, and 4 hours of PDBu stimulation. Each group consisted of three biological replicates.
