Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA108369 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Over activation of the aryl hydrocarbon receptor (AhR) by TCDD results ampng other phenotypes in severe thymic atrophy accompanied by immunosuppression. The link between thymic atrophy, skewed thymocyte differntiation and immunosuppression is still not fully resolved. This study investigates the TCDD elicted exprssion changes in the ET, cortical thymus epithelial cell line. Keywords: TCDD, AhR, thymic epithelial cells, thymic involution, thymus atrophy
2008-12-31 | GSE10168 | GEO
Project description:Over activation of the aryl hydrocarbon receptor (AhR) by TCDD results ampng other phenotypes in severe thymic atrophy accompanied by immunosuppression. The link between thymic atrophy, skewed thymocyte differntiation and immunosuppression is still not fully resolved. This study investigates the TCDD elicted exprssion changes in the ET, cortical thymus epithelial cell line. Keywords: TCDD, AhR, thymic epithelial cells, thymic involution, thymus atrophy ET cells were grown to 80-90% confluence and treated with 5nM TCDD or solvent control (1,4-Dioxane, 0,05%V). 2h,4h and 6h after treatment, RNA was isolated using TRIzol and gene expression measured. All experiments wer done in biological duplicates.
2008-12-30 | E-GEOD-10168 | biostudies-arrayexpress
Project description:Comparison of expression profiles detected in A549 cells exposed to DMSO, TCDD, and BaP for 2w Exposure to persistent ligands of aryl hydrocarbon receptor (AhR) has been found to cause lung cancer in experimental animals and lung adenocarcinomas are often associated with enhanced AhR expression and aberrant AhR activation. In order to better understand the action of toxic AhR ligands in lung epithelial cells, we performed global gene expression profiling in order to analyse TCDD- induced changes in A549 transcriptome, and compare them with changes in transcriptome of A549 cells exposed to BaP for 2w.
2019-09-01 | GSE122733 | GEO
Project description:Comparison of expression profiles detected in A549 cells exposed to DMSO, TCDD, CH223191 or their combination Exposure to persistent ligands of aryl hydrocarbon receptor (AhR) has been found to cause lung cancer in experimental animals and lung adenocarcinomas are often associated with enhanced AhR expression and aberrant AhR activation. In order to better understand the action of toxic AhR ligands in lung epithelial cells, we performed global gene expression profiling in order to analyse TCDD- induced changes in A549 transcriptome, both sensitive and non-sensitive to co-treatment with AhR inhibitor CH223191. Comparison of our data with results from previously reported microarray and ChIP-seq experiments enabled us i) to identify candidate genes, which expression status acutely (e.g. Aldh1a3, Grem1, Hipk2, Tiparp), or with a delay (Cdh1, Dkk1, Bmp6), reflects exposure of lung cancer cells to TCDD, ii) to predict processes/pathways (e.g. ER stress, Wnt/β-cat, IFNɣ, EGFR/Erbb1), as well as iii) putative TFs (e.g. Stat, AP1, E2F1, TCF4), which may be implicated in adaptive response of lung cells to TCDD-induced AhR activation.
2018-01-25 | GSE109576 | GEO
Project description:The aryl hydrocarbon receptor (AHR) is a ligand activated transcription factor that regulates the expression of xenobiotic detoxification genes and is a critical mediator of gene-environment interactions. In addition, many AHR target genes that have been identified by genome-wide profiling have morphogenetic functions, suggesting that AHR activation may play a role in embryonic development. To address this hypothesis, we studied the consequences of AHR activation by TCDD, its prototypical ligand, during spontaneous mouse ES cell differentiation into contractile cardiomyocytes. Treatment with TCDD or shRNA-mediated AHR knockdown significantly decreased the ability of cardiomyocytes to contract and the expression of cardiac markers in these cells. An AHR-positive embryonic stem cell lineage was generated that expressed puromycin resistance and eGFP under the control of the AHR-responsive Cyp1a1 promoter. Cells of this lineage were over 90% pure and expressed AHR as well as cardiomyocyte markers. Analysis of temporal trajectories of global gene expression in these cells shows that activation of the AHR/TCDD axis disrupts the concerted expression of genes that regulate multiple signaling pathways involved in cardiac and neural morphogenesis and differentiation, including dozens of genes encoding homeobox transcription factors and Polycomb and Trithorax Group genes. More than 50% of the homeobox factors so regulated do not have AhRE sites in their promoters, indicating that AHR activation may establish a complex regulatory network that reaches beyond direct AHR signaling and is capable of disrupting various aspects of embryonic development, including cardiomyocyte differentiation. mRNA profiles of WT and selected AHR positive cells at different differentiation days treated with and without TCDD in duplicates
2013-06-15 | E-GEOD-47964 | biostudies-arrayexpress
Project description:Exposures to dioxin, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) cause a wide array of toxicities in vertebrates and is mostly considered to be mediated through the inappropriate activation of the aryl hydrocarbon receptor (Ahr) signaling pathway. Although transcriptional regulation by Ahr is widely studied, the molecular mechanisms responsible for the adverse outcomes after Ahr activation are largely unknown. To identify the important events downstream of AHR activation that play an actual role in the toxic responses, we employed the zebrafish caudal fin regeneration models since Ahr activation blocks the regenerative process. Zebrafish regenerate their caudal fins by an orchestrated progression of cell migration, differentiation and proliferation controlled by a multitude of signaling pathways. This complex process was exploited as an in vivo platform to identify cross talk between Ahr and other signaling pathways. Global genomic analysis was performed in the larval regenerating fin tissue after exposure to TCDD in order to identify genes differentially regulated after Ahr activation. Comparative toxicogenomic analysis revealed that both adult and larval fins respond to TCDD during regeneration with mis-expression of Wnt signaling pathway members and Wnt target genes. Experiment Overall Design: The caudal fin of zebrafish larvae at 2days post fertilization were amputated and exposed to vehicle control alone or TCDD. Regenerating fins were isolated at 2and 3 days post amputation. Three replicates were collected at each time point. 150 fins were pooled to comprise one replicate.
2008-04-07 | E-GEOD-10184 | biostudies-arrayexpress
Project description:Transcriptional activation of AhR pathway in keratinocytes
| PRJNA92433 | ENA
Project description:AHR ChIP-Seq of female mouse liver following 2 hour TCDD exposure
| PRJNA382532 | ENA
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:The goal of this project was to determine how AhR activity in hepatocytes and HSCs impact liver fibrosis by studying mice with AhR-deficient hepatocytes (AhRΔHep) or AhR-deficient HSCs (AhRΔHSC) during TCDD-induced liver fibrosis as measured by evidence of steatosis, inflammation, HSC activation, and collagen deposition. Overall, our studies indicate that chronic TCDD exposure increases AhR signaling in hepatocytes that result in indirect HSC activation and the development of liver steatosis, whereas hepatic inflammation do not appear to play a major role.
2023-11-01 | GSE200710 | GEO