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ABSTRACT:
PROVIDER: PRJNA786610 | ENA |
REPOSITORIES: ENA
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Project description:The aryl hydrocarbon receptor (AHR) mediates the toxic effects of environmental contaminants, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Frogs are very insensitive to the toxic effects of TCDD.
2009-06-24 | GSE16670 | GEO
Project description:We report mRNA sequencing from decidual stromal cells after 24 hours and 6 days treatment with Aryl Hydrocarbon Receptor (AHR) activators 100 µM L-kynurenine or 10 nM TCDD (2,3,7,8-Tetrachlorodibenzo-p-dioxin)
2019-06-01 | GSE114552 | GEO
Project description:The aryl hydrocarbon receptor (AHR) is a ligand activated transcription factor that mediates the toxic effects of the environmental contaminant, dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin; TCDD). Dioxin causes a diverse range of toxic responses, including hepatic damage and lethal wasting syndrome; however, the mechanisms of dioxin-induced toxicity are still unknown. Here we show that the loss of TCDD-inducible poly(ADP-ribose) polymerase (TIPARP; ARTD14), an ADP-ribosyltransferase and AHR repressor, increases sensitivity to dioxin-induced toxicity and lethality. Tiparp-/- mice treated with a single injection of 100 mg/kg dioxin display an accelerated lethal wasting syndrome with no Tiparp-/- mice surviving beyond day 5; all Tiparp+/+ mice survived up to 30 days post treatment. Tiparp-/- mice displayed dramatic increases in liver steatosis and hepatotoxicity. At the molecular level, TIPARP selectively ADP-ribosylates AHR, but not AHR nuclear translocator (ARNT) and the Tiparp-dependent repression of AHR is reversed by the ADP-ribosylase and macrodomain containing protein MacroD1, but not MacroD2. These results describe previously unidentified roles for Tiparp, MacroD1, and ADP-ribosylation in AHR signaling, dioxin toxicity and lethality. 12 samples were analyzed. There were 4 treatment groups and each treatment group was done in triplicate. Gene expression changes were determine in hepatic RNA isolated from (1) corn oil treated C57BL/6;129Sv mice; (2) 30 ug/kg/bw 2,3,7,8-Tetrachlorodibenzo-p-dioxin C57BL/6;129Sv mice; (3) corn oil treated C57BL/6;129Sv Tiparp-/- mice; and (4) 30 ug/kg/bw 2,3,7,8-Tetrachlorodibenzo-p-dioxin C57BL/6;129Sv Tiparp-/- mice
2015-05-14 | E-GEOD-61534 | biostudies-arrayexpress
Project description:Aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor, which mediates the effects of various environmental contaminants, like polycyclic and halogenated aromatic hydrocarbons, including the most potent agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), in multiple tissues. Recent advances in AHR biology have underlined its importance in cells with high developmental potency, including pluripotent stem cells. Nonetheless, there is little data on AHR expression and its role during the initial stages of stem cell differentiation. The purpose of this study was to investigate the temporal pattern of AHR expression during directed differentiation of human embryonic stem cells (hESC) into neural progenitor, early mesoderm and definitive endoderm cells. Additionally, we studied the effect of AHR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on gene expression profile in hESCs and differentiated cells by RNA-seq, accompanied by identification of AHR binding sites by ChIP-seq and epigenetic landscape analysis by ATAC-seq. . We show that AHR is differentially regulated in distinct lineages, provide evidence that TCDD impairs differentiation of hESCs and identify novel potential AHR target genes which expand our understanding on the role of this protein in different cell types.
2020-12-03 | GSE160981 | GEO
Project description:Aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor, which mediates the effects of various environmental contaminants, like polycyclic and halogenated aromatic hydrocarbons, including the most potent agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), in multiple tissues. Recent advances in AHR biology have underlined its importance in cells with high developmental potency, including pluripotent stem cells. Nonetheless, there is little data on AHR expression and its role during the initial stages of stem cell differentiation. The purpose of this study was to investigate the temporal pattern of AHR expression during directed differentiation of human embryonic stem cells (hESC) into neural progenitor, early mesoderm and definitive endoderm cells. Additionally, we studied the effect of AHR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on gene expression profile in hESCs and differentiated cells by RNA-seq, accompanied by identification of AHR binding sites by ChIP-seq and epigenetic landscape analysis by ATAC-seq. . We show that AHR is differentially regulated in distinct lineages, provide evidence that TCDD impairs differentiation of hESCs and identify novel potential AHR target genes which expand our understanding on the role of this protein in different cell types.
2020-12-03 | GSE160980 | GEO
Project description:Aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor, which mediates the effects of various environmental contaminants, like polycyclic and halogenated aromatic hydrocarbons, including the most potent agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), in multiple tissues. Recent advances in AHR biology have underlined its importance in cells with high developmental potency, including pluripotent stem cells. Nonetheless, there is little data on AHR expression and its role during the initial stages of stem cell differentiation. The purpose of this study was to investigate the temporal pattern of AHR expression during directed differentiation of human embryonic stem cells (hESC) into neural progenitor, early mesoderm and definitive endoderm cells. Additionally, we studied the effect of AHR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on gene expression profile in hESCs and differentiated cells by RNA-seq, accompanied by identification of AHR binding sites by ChIP-seq and epigenetic landscape analysis by ATAC-seq. . We show that AHR is differentially regulated in distinct lineages, provide evidence that TCDD impairs differentiation of hESCs and identify novel potential AHR target genes which expand our understanding on the role of this protein in different cell types.
2020-12-03 | GSE160935 | GEO
Project description:Aryl hydrocarbon receptor ChIP-Seq performed in livers of female mice gavaged with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for 2hrs
2017-04-12 | GSE97636 | GEO
Project description:Aryl hydrocarbon receptor ChIP-Seq performed in livers of male mice gavaged with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for 2hrs
2017-04-12 | GSE97634 | GEO
Project description:The aryl hydrocarbon receptor (AHR) mediates the toxic effects of environmental contaminants, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Frogs are very insensitive to the toxic effects of TCDD. Experiment Overall Design: XLK-WG cells (ATCC) were grown to ~90% confluence in RPMI-1640 media supplemented with 20% FBS at 29 degrees and 5% CO2. Cells were subsequently exposed to 100 nM TCDD, FICZ, or DMSO vehicle (0.25%) for 3 hr prior to extraction of total RNA. Experiment Overall Design: Study included three complete biological replicates of each treatment.
2009-07-05 | E-GEOD-16670 | biostudies-arrayexpress
Project description:Dioxin and dioxin-related polychlorinated biphenyls are potent toxicants with association with developmental heart defects and congenital heart diseases. However, the underlying mechanism of their developmental toxicity is not fully understood. Further, different animals show distinct susceptibility and phenotypes after exposure, suggesting possible species-specific effects. Using a human embryonic stem cell (ESC) cardiomyocyte differentiation model, we examined the impact, susceptible window, and dosage of 2,3,7,8‑tetrachlorodibenzo‑p‑dioxin (TCDD) on human cardiac development. We showed that treatment of human ESCs with TCDD at the ESC stage inhibits cardiomyocyte differentiation, and the effect is largely mediated by the aryl hydrocarbon receptor (AHR). We further identified genes that are differentially expressed after TCDD treatment by RNA-sequencing, and genomic regions that are occupied by AHR by chromatin immunoprecipitation and high-throughput sequencing. Our results support the model that TCDD impairs human ESC cardiac differentiation by promoting AHR binding and repression of key mesoderm genes. More importantly, our study demonstrates the toxicity of dioxin in human embryonic development and uncovered a novel mechanism by which dioxin and AHR regulates lineage commitment. It also illustrates the power of ESC-based models in the systematic study of developmental toxicology.
2018-10-31 | GSE122002 | GEO