Figure 4
From: Loss of NR2E3 represses AHR by LSD1 reprogramming, is associated with poor prognosis in liver cancer
Effects of NR2E3 depletion on the transcriptional and epigenetic status of AHR gene promoter, AHR expression, and AHR-mediated responsiveness in vivo. (a) NR2E3 and AHR protein levels were determined using three individual wild-type (WT) and Nr2e3rd7/rd7 (Rd7) mice liver tissue lysates by immunoblotting. (b) Representative images of immunohistological staining of NR2E3 and AHR in WT and Nr2e3rd7/rd7 liver tissues (left) and with AHR (right). Long arrows: central vein; short arrows: pericental hepatocytes (c,d) Effects of NR2E3 loss on the transcriptional and epigenetic status of the AHR proximal promoter region in WT and Rd7 mice, as determined by in vivo ChIP-PCR analysis. (e) Significant decrease in the induction levels of CYP1A1 and CYP1A2 in Rd7 (N = 4) mice than in WT mice (N = 4; injected intraperitoneally with 0, 1, and 10 μg/kg of TCDD). (f) Measurement of ethoxyresorufin-O-deethylase (EROD) activity associated with CYP1A enzyme activities in TCDD-treated WT and Rd7 liver tissues. 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.
