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Aryl Hydrocarbon Receptor Ligands Present In The Environment Impact Human Trophoblast Cell Development

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE246513 | GEO | 2024/10/08

REPOSITORIES: GEO

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Aryl Hydrocarbon Receptor Ligands Present In The Environment Impact Human Trophoblast Cell Development [STEM]

Project description:TCDD do not activate AHR signaling in rat TS cells but do so in human TS cells with different biological outcomes. TCDD activates AHR signaling, stimulates the synthesis of 2 methoxy estradiol (2ME), a biologically active catechol estrogen, without directly affecting human TS cell differentiation. TCDD actions on human TS cells were dependent upon AHR signaling.

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Aryl Hydrocarbon Receptor Ligands Present In The Environment Impact Human Trophoblast Cell Development [ST3D]

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Aryl Hydrocarbon Receptor Ligands Present In The Environment Impact Human Trophoblast Cell Development [EVT]

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Aryl Hydrocarbon Receptor Ligands Present In The Environment Impact Human Trophoblast Cell Development

Project description:Aryl Hydrocarbon Receptor Ligands Present In The Environment Impact Human Trophoblast Cell Development

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Aryl Hydrocarbon Receptor Ligands Present In The Environment Impact Human Trophoblast Cell Development [ST3D]

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Zebrafish larvae aryl hydrocarbon receptor ligands and inhibitor

Project description:Wild type zebrafish (AB strain, https://zfin.org/action/genotype/view/ZDB-GENO-960809-7) were set up for mating overnight, in 3:2 ratios, females and males, respectively. Fertilized embryos from wildtype zebrafish AB strain were used for all experiments and kept in Embryo medium (E3, 5 mM NaCl, 0.17 mM KCl, 0.33 mM CaCl2, 0.33 mM MgSO4) in an incubator at 28ºC. At 1dpf, larvae were manually dechorionated under a stereomicroscope. At 2dpf, zebrafish larvae were divided randomly into the different experimental groups, at a density of 12 larvae per well of a 12 well plate (Corning) in 1.5mL of E3. Three biological replicates of 12 larvae per condition were exposed to different conditions for 4 hours at 28 ºC: DMSO; DMSO + CH223191 (5mM); 3-o-C12-L-HSL (50mM); 3-o-C12-L-HSL (50mM) + CH223191 (5 mM ); 1-hydroxyphenazine (1-HP, 5mM); 1-HP (5mM) + CH223191(5mM) and 1-HP (5mM) + 3-o-C12-L-HSL (50mM).To mention, in experiments using the Aryl hydrocarbon Receptor inhibitor CH223191, larvae were pre-exposed to 5uM of the inhibitor for 2h prior to the start of the experiment and the inhibitor was kept during the experiment. After the desired exposure to diverse ligands, larvae were euthanized with Tricaine (MS-222, 300 µg/mL) and placed in Trizol for RNA isolation. The same experimental layout was performed 5 times, and samples were subjected to microarray hybridization and analysis.

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Ginsenosides are novel naturally-occurring aryl hydrocarbon receptor ligands.

Project description:The aryl hydrocarbon receptor (AHR) is a ligand-dependent transcription factor that mediates many of the biological and toxicological actions of structurally diverse chemicals. In this study, we examined the ability of a series of ginsenosides extracted from ginseng, a traditional Chinese medicine, to bind to and activate/inhibit the AHR and AHR signal transduction. Utilizing a combination of ligand and DNA binding assays, molecular docking and reporter gene analysis, we demonstrated the ability of selected ginsenosides to directly bind to and activate the guinea pig cytosolic AHR, and to stimulate/inhibit AHR-dependent luciferase gene expression in a recombinant guinea pig cell line. Comparative studies revealed significant species differences in the ability of ginsenosides to stimulate AHR-dependent gene expression in guinea pig, rat, mouse and human cell lines. Not only did selected ginsenosides preferentially activate the AHR from one species and not others, mouse cell line was also significantly less responsive to these chemicals than rat and guinea pig cell lines, but the endogenous gene CYP1A1 could still be inducted in mouse cell line. Overall, the ability of these compounds to stimulate AHR signal transduction demonstrated that these ginsenosides are a new class of naturally occurring AHR agonists.

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