Fig. 5: REDD1 elicits adipocyte differentiation and macrophage inflammation through NF-κB activation.
From: REDD1 promotes obesity-induced metabolic dysfunction via atypical NF-κB activation
a–c Representative oil red-O (ORO)-stained images of WT and Redd1−/− SVF cells (a), shControl (shC)- or sh-Redd1-transfected 3T3-L1 cells (b), and WT (Redd1fl/fl, Rfl/fl) and Redd1ΔAdipoq (RΔAdipoq) SVF cells (c) when cultured in differentiation medium (MDI) and quantification of relative ORO intensity (n = 4). d–f, Expression levels of adipogenic genes (d), REDD1 (e), and lipogenic genes (f) in Rfl/fl and RΔAdipoq SVF cells cultured in MDI medium and quantification of relative ORO intensity (n = 4). g Assessment of NF-κB–Luc activity in 3T3-L1 cells transfected either with siRNA for control, Ikka, Ikkb, or NF-κB p65 (p65) or with pcDNA3.1/His-Ikba (n = 5). h, i Representative images and realative quantification of ORO-stained images (h) and expression levels of Pparg and Cebpa (i) in 3T3-L1 cells infected with control adenovirus (Ad-C) or adenoviral Redd1 (Ad-R) after transfection with vector alone or pcDNA3.1/His-Ikba (n = 4). j NF-κB–Luc activity in mouse peritoneal macrophages infected with Ad-C or Ad-Redd1 (n = 4). k Cytokine production in mouse peritoneal macrophages infected with Ad-C or Ad-Redd1 (n = 5). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using one-way ANOVA (g, h) and two-way ANOVA (a, i) followed by the Holm–Sidak post hoc test and an unpaired two-tailed t-test (b–f, j, k). Source data are provided as a Source Data file.
