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. 2017 Sep 6;7:10662. doi: 10.1038/s41598-017-11106-2

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Restoration of AHR expression by administration of a chemical inhibitor of LSD1 to RD7 mice. (a,b) Rd7 mice were intraperitoneally injected with 15 mg/kg of SP2509 (twice with a 24-h interval). After 48 h, the livers were harvested, homogenized, and the AHR protein levels were analyzed by immunoblotting. AHR mRNA levels were determined by qRT-PCR (c) Representative images of immunostaining of Rd7 mice liver tissues treated with and without SP2509. (d) Effects of NR2E3 loss on the transcriptional and epigenetic status of the AHR proximal promoter region in Rd7 mice liver tissues treated with and without SP2509, determined by in vivo ChIP-PCR. (e) A proposed model for the role of NR2E3 in the transcriptional and epigenetic status of the AHR promoter. Results are means ± SE for at least two or three independent experiments with three replicates per experiment, and significantly (P < 0.05) increased (*) or reduced (**) responses are indicated.