Activation of MR but not GR enhanced TNFR2 expression by a NF-κB-dependent mechanism
. BV-2 cells were treated for 24 h with corticosterone (A, C, D, E), 11-dehydrocorticosterone (F), dexamethasone (B), or aldosterone (C-F), in the presence or absence of 1 μM spironolactone (A, C, D), 1 μM RU-486 (A, B), or 250 nM NF-κB inhibitor Cay-10512 (C, E). The impact of 11β-HSD1 was assessed by co-incubation of cells with 1 μM T0504. TNFR2 mRNA was quantitated by real-time RT-PCR. Data (mean ± SD from three independent experiments) represent ratios of TNFR2 mRNA to GAPDH control mRNA from treated cells normalized to the values obtained from cells incubated with vehicle (DMSO). For western blot analysis (D, E, F) equal protein amounts were loaded and probed for TNFR2 with actin as a loading control. A representative blot from three independent experiments is shown. ***P <0.005.