Effect of caMEKK1 on NF-κB and RAR activities. Chondrocytes were co-transfected with a constitutively active mitogen-activated protein kinase kinase kinase (caMEKK)1 expression vector and (a) nuclear factor-κB (NF-κB) or (b) retinoic acid response element (RARE) reporter vectors. Cells were then treated with or without tumour necrosis factor (TNF)-α (30 ng/ml) and/or all-trans retinoic acid (atRA; 100 nmol/l) for 24 hours. Panel a: caMEKK1 increased basal NF-κB activity and this level was not further increased by TNF-α. atRA had no effect on the level of caMEKK1-induced NF-κB activity. Panel b: atRA significantly increased RAR activity. Co-transfection with the IκB-2N expression vector inhibited NF-κB activity and further increased atRA-induced RAR activity (b, P < 0.001). Data are ratios of NF-κB- or RAR-regulated firefly luciferase units to constitutive SV40-regulated renilla luciferase units, and are means ± standard error (n = 3) from a single experiment, representative of three independent experiments. Data were evaluated by one-way analysis of variance and Tukey's multiple comparisons tests. Unlabelled bars or bars labelled with the same lower case letters are not significantly different (P > 0.05).
Rockel et al. Arthritis Research & Therapy 2008 10:R3 doi:10.1186/ar2349