Similar Datasets
Project description:miRNA profiling of lung epithelial cells (BEAS-2B cells) exposed to manganese (Mn)
| PRJNA1034564 | ENA
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: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
2017-01-10 | GSE93329 | GEO
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
2019-03-07 | GSE127962 | GEO
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:Methotrexate (MTX) has been widely used for the treatment of a variety of tumors as well as for inflammatory diseases and rheumatoid arthritis (RA). MTX-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 MTX-induced pulmonary toxicity gene expression in BEAS-2B cells, huma bronchial cell line, by microarray. The expression of these genes are potential biomarker of methotrexate-induced pulmonary toxicity. Also, We provide a clue about mechanism of pulmonary toxic action by these clinical chemotherapeutic agents. Keywords: 48h treatment, 0.144uM (dose), MTX
2008-12-06 | GSE9815 | GEO
Project description:Methotrexate (MTX) has been widely used for the treatment of a variety of tumors as well as for inflammatory diseases and rheumatoid arthritis (RA). MTX-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 MTX-induced pulmonary toxicity gene expression in BEAS-2B cells, huma bronchial cell line, by microarray. The expression of these genes are potential biomarker of methotrexate-induced pulmonary toxicity. Also, We provide a clue about mechanism of pulmonary toxic action by these clinical chemotherapeutic agents. Experiment Overall Design: BEAS-2B cells were seeded and after incubation for 24 h at 37C, the cells were treated with 0.144 ?M(IC20) MTX 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.
2008-12-12 | E-GEOD-9815 | biostudies-arrayexpress
Project description:RNAseq was performed using cerebellum tissue of mice with either normal (35 ppm) or Mn-deficient (0 ppm) diet
2020-11-25 | GSE147364 | GEO
Project description:We used mass spectrometry to profile changes in metabolites, proteins, and phosphorylation in silica-exposed BEAS-2B epithelial cells.
2022-07-28 | PXD035608 |
Project description:Despite its necessity, manganese (Mn) can causes phytotoxicity when present in excess. Stylo (Stylosanthes) is a dominant tropical legume with high Mn adaptability, but its Mn tolerance mechanisms are not well documented. This study integrated both physiological and transcriptome analyses of stylo in response to excess Mn toxicity. Results showed that stylo growth was decreased by excess Mn higher than 200 µM, as reflected by reductions in leaf chlorophyll and plant dry weight. Increases in enzyme activities of peroxidase (POD), ascorbate peroxidase (APX) and phenylalanine ammonia-lyase (PAL) and concentrations of secondary metabolites, including total phenols, flavonoids, tannins and anthocyanidins, were observed in stylo leaves at high Mn stress. Transcriptome analysis in stylo leaves resulted in identification of 2,471 up-regulated and 1,623 down-regulated genes under excess Mn toxicity. Among them, a set of differentially expressed genes (DEGs) involved in secondary metabolism, including PAL, chalcone synthase (CHS), chalcone isomerase (CHI) and flavonol synthase (FLS), were up-regulated in stylo under Mn toxicity, which were closely associated with the accumulation of secondary metabolites, suggesting that activation of secondary metabolism and corresponding gene expression might be important for stylo adaptation to Mn toxicity. Furthermore, a group of DEGs encoding transcription factors, such as genes belonged to C2H2 zinc finger transcription factor, WRKY, MYB and AP2 family, may be involved in stylo responses to Mn toxicity. Taken together, this study suggests that enhancing defense response and secondary biosynthesis pathway is adaptive strategy of stylo during Mn exposure, which might be regulated by complex transcriptional regulatory networks.
2020-12-08 | GSE147431 | GEO