Project description:Human bronchial epithelial cell line Beas-2B were infected with Streptococcus pneumoniae at Multiplicity of Infection (MOI) of 0.5 and 1 or treated with lipoteichonic acid (LTA) for 9 and 16 h. The mRNA profile changes upon infection shall be determined to investigate Streptococci pathogenesis.
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:Time course transcriptomic profiling of human bronchial epithelial cell BEAS-2B exposed to a single dose of diesel and biomass ultrafine particles
Project description:We used mass spectrometry to profile changes in metabolites, proteins, and phosphorylation in silica-exposed BEAS-2B epithelial cells.
Project description:We established chromate transformed cell lines by chronic exposure of normal human bronchial epithelial BEAS-2B cells to low doses of hexavalent chromium followed by anchorage-independent growth. The gene expression profiles were analyzed in the established cell lines. The gene expression profiles from six chromate transformed cell lines were remarkably similar to each other yet differed significantly from that of either control cell line or normal Beas-2B cells. A total of 409 differentially expressed genes were identified in chromate transformed cells compared to control cells.
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.
Project description:BEAS-2B cells are human bronchial epithelial cells, and often used as a in vitro model for the detection of potential pulmonary toxicity of chemicals. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes after treated with chemical substance
Project description:We established chromate transformed cell lines by chronic exposure of normal human bronchial epithelial BEAS-2B cells to low doses of hexavalent chromium followed by anchorage-independent growth. The gene expression profiles were analyzed in the established cell lines. The gene expression profiles from six chromate transformed cell lines were remarkably similar to each other yet differed significantly from that of either control cell line or normal Beas-2B cells. A total of 409 differentially expressed genes were identified in chromate transformed cells compared to control cells. We analyzed gene expression profiles from 10 cell lines ( six chromated transformed cells lines, three control cell lines, and parental BEAS-2B cells) using Affymetrix Human Gene 1.0 ST array. No techinical replicates were performed.
Project description:BEAS-2B cells are human bronchial epithelial cells, and often used as a in vitro model for the detection of potential pulmonary toxicity of chemicals. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes after treated with chemical substance
Project description:Our previous studies proved that both epithelial inflammation and sub-epithelial remodeling were linked to deregulated PRMT1 expression in asthma patients. This sncRNA-seq data from the BEAS-2B cell line after over-expressed PRMT1 for 24h.