ArticlePloS one2017
Loss of liver-specific and sexually dimorphic gene expression by aryl hydrocarbon receptor activation in C57BL/6 mice.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Spatial transcriptomic profiling uncovers the molecular effects of the neurotoxicant polychlorinated biphenyls (PCBs) in the brains of adult mice.Molecular psychiatry · 2026Article
- Subchronic low dose dioxin exposure disrupts hepatic and metabolic homeostasis in a sex- and diet-dependent manner.Current research in toxicology · 2026Article
- Maternal Exposure to Ozone During Implantation Promotes a Feminized Transcriptomic Profile in the Male Adolescent Liver.Endocrinology · 2025Article
- Low dose exposure to dioxins alters hepatic energy metabolism and steatotic liver disease development in a sex-specific manner.Environment international · 2024Article
- Gender- and Age-Group Specific Association of Persistent Organic Pollutants (POPs) Exposure with Diabetes Mellitus: Korean National Environmental Health Survey (KoNEHS) 2015-2017.Environment & health (Washington, D.C.) · 2024Article
- TCDD dysregulation of lncRNA expression, liver zonation and intercellular communication across the liver lobule.Toxicology and applied pharmacology · 2023Article
- RISING STARS: Sex differences in toxicant-associated fatty liver disease.The Journal of endocrinology · 2023Review
- Sex, Nutrition, and NAFLD: Relevance of Environmental Pollution.Nutrients · 2023Review
- Single-cell transcriptomics shows dose-dependent disruption of hepatic zonation by TCDD in mice.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- TCDD dysregulation of lncRNA expression, liver zonation and intercellular communication across the liver lobule.bioRxiv : the preprint server for biology · 2023Article
- The environmental pollutant, polychlorinated biphenyl 126, alters liver function in a rodent model of alcohol-associated liver disease.Alcohol, clinical & experimental research · 2023Article
- Genome-Wide ChIPseq Analysis of AhR, COUP-TF, and HNF4 Enrichment in TCDD-Treated Mouse Liver.International journal of molecular sciences · 2022Article
- Regulation of Sexually Dimorphic Expression of Major Urinary Proteins.Frontiers in physiology · 2022Review
- The aryl hydrocarbon receptor as a model PAS sensor.Toxicology reports · 2022Review
- Aryl Hydrocarbon Receptor (AhR) Activation by 2,3,7,8-Tetrachlorodibenzo-International journal of molecular sciences · 2021Article
- Single-Nuclei RNA Sequencing Assessment of the Hepatic Effects of 2,3,7,8-Tetrachlorodibenzo-p-dioxin.Cellular and molecular gastroenterology and hepatology · 2021Article
- 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) dysregulates hepatic one carbon metabolism during the progression of steatosis to steatohepatitis with fibrosis in mice.Scientific reports · 2020Article
- The Ancestral Environment Shapes Antiviral CD8iScience · 2019Article
- Pseudomonas aeruginosa-derived pyocyanin reduces adipocyte differentiation, body weight, and fat mass as mechanisms contributing to septic cachexia.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2019Article
- Effects of Aryl Hydrocarbon Receptor Deficiency on PCB-77-Induced Impairment of Glucose Homeostasis during Weight Loss in Male and Female Obese Mice.Environmental health perspectives · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The aryl hydrocarbon receptor (AhR) is a highly conserved transcription factor that mediates a broad spectrum of species-, strain-, sex-, age-, tissue-, and cell-specific responses elicited by structurally diverse ligands including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Dose-dependent effects on liver-specific and sexually dimorphic gene expression were examined in male and female mice gavaged with TCDD every 4 days for 28 or 92 days. RNA-seq data revealed the coordinated repression of 181 genes predominately expressed in the liver including albumin (3.7-fold), α-fibrinogen (14.5-fold), and β-fibrinogen (17.4-fold) in males with corresponding AhR enrichment at 2 hr. Liver-specific genes exhibiting sexually dimorphic expression also demonstrated diminished divergence between sexes. For example, male-biased Gstp1 was repressed 3.0-fold in males and induced 4.5-fold in females, which were confirmed at the protein level. Disrupted regulation is consistent with impaired GHR-JAK2-STAT5 signaling and inhibition of female specific CUX2-mediated transcription as well as the repression of other key transcriptional regulators including Ghr, Stat5b, Bcl6, Hnf4a, Hnf6, Foxa1/2/3, and Zhx2. Attenuated liver-specific and sexually dimorphic gene expression was concurrent with the induction of fetal genes such as alpha-fetoprotein. The results suggest AhR activation causes the loss of liver-specific and sexually dimorphic gene expression producing a functionally "de-differentiated" hepatic phenotype.
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Registered trials
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