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. 2010 Feb 15;24(4):381–395. doi: 10.1101/gad.545110

Figure 1.

Figure 1.

LRH-1 and LXRs inhibit hepatic APR gene expression. (A–C) The potential of LRH-1 (GR8470) and LXR (GW3965) agonists to repress cytokine-induced APR gene expression was analyzed in human primary hepatocytes. Hepatocytes were pretreated with vehicle (DMSO), GR8470 (10 μM), or GW3965 (2 μM) for 24 h and stimulated with 10 nM IL1β + IL6 for 16 h. Haptoglobin, SAA, and PAI-1 mRNA levels were quantified by qPCR. Data are presented as mean ± SD of three independent experiments. (D) IL1β + IL6 induce the dissociation of N-CoR or SMRT corepressor complexes from APR promoters. Huh7 cells were stimulated with 10 nM IL1β + IL6 for 1 h. Protein recruitment to APR promoters was analyzed by ChIP. (E,F) Activation of LRH-1 (E) or LXR (F) prevents the dissociation of N-CoR complexes from the haptoglobin promoter. Huh7 cells were pretreated by GR8470 (10 μM) or GW3965 (2 μM) and treated with 10 nM IL1β + IL6 for 1 h. Protein recruitment was analyzed by ChIP and re-ChIP.