Figure 7.

Cholesterol selectively regulates GR transactivation in vivo. Serum samples from WT and ApoE ^−/− mice (eight animals per group) were analysed for levels of cholesterol, HDL and triglycerides (A). Morning (0700 h) and evening (1900 h) serum samples from ApoE ^−/− mice (16 animals per group) were assayed for corticosterone (B). WT and ApoE ^−/− mice were subjected to a dexamethasone (Dex) suppression test. Mice (eight animals per group) were given i.p. injection of Dex (1 mg/kg) and then serum collected 4 h later (1900 h). Serum samples were assayed for corticosterone (C). WT and ApoE ^−/− mice (five animals per group) were given i.p. injection of Dex (1 mg/kg) and then livers collected 4 h later. Livers were analysed for GR expression by immunoblot (D). Blots show samples from three different animals. Livers were also analysed for induction of GR target genes MT1, PER1, and FKBP5 (E), DUSP1, NFKBIA, and GILZ (F) by qRT-PCR (all normalised to GAPDH). Graphs show mean±s.e.m. *P<0.05 and **P<0.01. NS, not significant.