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Cited by 212

Aryl hydrocarbon receptor-dependent liver development and hepatotoxicity are mediated by different cell types

Walisser, Jacqueline A., Glover, Edward, Pande, Kalyan, Liss, Adam L., Bradfield, Christopher A.·2005·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.0504757102
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Abstract

The aryl hydrocarbon receptor (AHR) plays a role in three areas of biology that include the adaptive metabolism of xenobiotics, the toxic responses associated with exposure to 2,3,7,8-tetrachlorodibenzo- p -dioxin (dioxin), and vascular remodeling of the developing embryo. To test the hypothesis that receptor signaling in different cell types is responsible for these aspects of AHR biology, we generated a conditional Ahr allele where exon 2 is flanked by loxP sites. Through the use of Cre -lox technology, we then investigated the role of AHR signaling in hepatocytes or endothelial cells in mediating prototypical endpoints of adaptive, toxic, or developmental signaling. Using this model, we provide evidence that AHR signaling in endothelial/hematopoietic cells is necessary for developmental closure of the ductus venosus, whereas AHR signaling in hepatocytes is necessary to generate adaptive and toxic responses of the liver in response to dioxin exposure. Taken together, these data illustrate the importance of cell-specific receptor signaling for the generation of distinct AHR-dependent physiological outcomes.

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  • TCDD toxicity and ductus venosus closure require AHR activation in hepatocytes and endothelial cells, respectively.

    “To this end, Ahrfx was crossed to hepatocyte-specific (CreAlb) or endothelial-specific (CreTek) Cre recombinase to demonstrate that TCDD toxicity and the closure of the DV require receptor activation in hepatocytes and endothelial cells, respectively (Kisanuki et al., 2001; Postic et al., 1999; Walisser et al., 2005).”

    From Rodent Genetic Models of Ah Receptor Signaling (2021) · cites this paper as Walisser et al., 2005

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Authors
Walisser, J. A., Glover, E., Pande, K., Liss, A. L., & Bradfield, C. A.
Affiliations
McArdle Laboratory for Cancer Research, University of Wisconsin Medical School, Madison, WI 53706
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
2005-11-21
Volume
102
Issue
49
Pages
17858-17863
ISSN
  • 0027-8424
  • 1091-6490
DOI
10.1073/pnas.0504757102
Cited by
212
References
5
Language
en

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