ABSTRACT: Cross-Species Comparisons of Transcriptomic Alterations in Human and Rat Primary Hepatocytes Exposed to 2,3,7,8-Tetrachlorodibenzo-p-dioxin: human samples
Project description:Cross-Species Comparisons of Transcriptomic Alterations in Human and Rat Primary Hepatocytes Exposed to 2,3,7,8-Tetrachlorodibenzo-p-dioxin
Project description:Cross-Species Comparisons of Transcriptomic Alterations in Human and Rat Primary Hepatocytes Exposed to 2,3,7,8-Tetrachlorodibenzo-p-dioxin: rat samples
Project description:A toxicogenomics approach was used to qualitatively and quantitatively compare the gene expression changes in human and rat primary hepatocytes exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Hepatocytes from five individual rats and five individual humans were exposed for 24 hours to 11 concentrations of TCDD ranging from 0.00001 nM to 100 nM and a vehicle control. Gene expression changes were analyzed using whole genome microarrays.
Project description:A toxicogenomics approach was used to qualitatively and quantitatively compare the gene expression changes in human and rat primary hepatocytes exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Hepatocytes from five individual rats and five individual humans were exposed for 24 hours to 11 concentrations of TCDD ranging from 0.00001 nM to 100 nM and a vehicle control. Gene expression changes were analyzed using whole genome microarrays.
Project description:We report the RNAseq-based transcriptome profiles of rat gestation day 20 dam liver, fetal male and female liver, fetal male pituitary, and fetal testis following in utero exposure to either 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or 2,3,7,8-tetrachlorodibenzofuran (TCDF). Two exposure models were examined: 1) pregnant rats exposed to either a dose response series of TCDD or TCDF from gestation day 6 - 20 or 2) pregnant rats exposed to a single dose of TCDD or TCDF on gestation day 15. These data support a mode-of-action for dioxin-induced rat male reproductive toxicity involving key events in both the fetal pituitary (reduced gonadotropin production) and fetal testis (reduced Leydig cell cholesterologenesis and steroidogenesis) which are hypothesized to decrease perinatal Sertoli cell proliferation and culminate in reduced spermatogenesis. The lack of a TCDF effect on proposed key events may be due to a higher rate of metabolic clearance relative to TCDD.
Project description:Expression profiles of Drosophila melanogaster in response to ionizing radiation, formaldehyde, toluene, and 2,3,7,8-tetrachlorodibenzo-p-dioxin.
Project description:Temporal comparison of transcriptomic alterations in human, mouse and rat primary B lymphocytes exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)
Project description:Comparison of expression profiles detected inundifferemtitated HepaRG cells exposed to DMSO, TCDD for 24h. The aryl hydrocarbon receptor (AhR) activation has been shown to stimulate proliferation, promote apoptosis or alter differentiation of adult rat liver progenitors. We investigated the impact of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-mediated AhR activation on a human model of bipotent liver progenitors, undifferentiated HepaRG cells. We used both intact undifferentiated HepaRG cells, and HepaRG cells with silenced Hippo pathway effectors, YAP1 and TAZ, which play key role(s) in tissue specific progenitor cell self-renewal and expansion, including liver, cardiac or respiratory progenitors.
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
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
