Regular ArticleInteractive Regulation of Ah and Glucocorticoid Receptors in the Synergistic Induction of Cleft Palate by 2,3,7,8-Tetrachlorodibenzo-p-dioxin and Hydrocortisone
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Proteomics and metabolic phenotyping define principal roles for the aryl hydrocarbon receptor in mouse liver
2021, Acta Pharmaceutica Sinica BCitation Excerpt :More data are clearly required to better understand interactions between the AHR and the transcription factors elucidated by the enrichment by IPF analysis. However, cross-regulation of Ahr and Gcr mRNA expression has been reported45. To our knowledge, miRs have not previously been associated with Ahr ablation, but they have been associated with PCB exposures.
Dioxin induction of transgenerational inheritance of disease in zebrafish
2014, Molecular and Cellular EndocrinologyCitation Excerpt :TCDD acts primarily through activation of the AHR/ARNT transcriptional regulator to alter gene expression, but cross talk with other signal transduction systems is suspected (Poland and Bradfield, 1992; Puga et al., 2009; Schmidt and Bradfield, 1996; Swanson and Bradfield, 1993). AHR activation by TCDD leads to altered expression of hormone receptors, receptor activators and repressors, metabolic enzymes needed for metabolism of xenobiotics and hormone synthesis and degradation, and other gene products required for normal development and endocrine function (Abbott et al., 1994; Beischlag et al., 2008; Gierthy et al., 1996; Massaad et al., 2002; Safe et al., 1998). Diseases in humans that have been associated with exposure to TCDD include cancer as well as chloracne, porphyria, and defects in the cardiovascular, skeletal, immune, central nervous system, hepatic and reproductive systems (Eskenazi et al., 2000; Guo et al., 2000; NAS-IOM, 2011; Pelclova et al., 2006; Warner et al., 2007, 2011).
A genomic and ecotoxicological perspective of DNA array studies in aquatic environmental risk assessment
2011, Aquatic ToxicologyCitation Excerpt :Yet, AhR interaction is key on the toxicity mechanism of dioxins, furans and PAHs, as mice devoid of these receptors become resistant to these compounds (Fernández-Salguero et al., 1996; Shimizu et al., 2000). These compounds elicit a broad range of physiological effects, including immune dysfunction, endocrine disruption, reproductive toxicity, developmental defects, and cancer in vertebrates (Abbott et al., 1994; Poland and Knutson, 1982; Safe, 1990). As in previous examples, toxicity appears through overcoming the capacity of the metabolism to detoxify the modified compounds, as oxidative processes generate reactive species (radicals, peroxides, etc.) that, if unquenched, may modify many structural components of the cell, including nucleic acids.
Convergence of Multiple Nuclear Receptor Signaling
2010, Comprehensive Toxicology: Second EditionGlucocorticoid and adrenalectomy effects on the rat aryl hydrocarbon receptor pathway depend on the dosing regimen and post-surgical time
2009, Chemico-Biological InteractionsCitation Excerpt :A functional impact of the altered level of AHR was observed as DEX pre-treatment enhanced induction of an AHR-activated luciferase reporter by TCDD and MC in Hepa-1 cells [22]. With respect to in vivo evidence regarding the glucocorticoid effect on AHR expression, Abbott et al. [23] showed that hydrocortisone increased AHR mRNA and protein in the embryonic mouse palate. A previous study in adrenalectomized (ADX) rats 1-week after surgery showed no alteration of AHR ligand-binding as measured by isoelectric focusing [24].