Fig. 1: Effects of 5-arylnicotinamides on ABCA1-mediated cholesterol efflux.

a Concentration-response of Cpd H on cholesterol efflux from human THP1 macrophages to different extracellular apolipoprotein acceptors. Data are represented as the mean ± SD from three independent experiments. b Cholesterol efflux assays were performed in normal human or Tangier (ABCA1-deficient) fibroblasts. Left panel, in normal fibroblasts both Cpd H and Cpd J (10 μM) increased cholesterol efflux to apoAI. Right panel, none of the test agents had an effect on cholesterol efflux to apoAI or other lipoprotein acceptors in fibroblasts genetically deficient for ABCA1. Data expressed as the mean ± SD from three independent experiments. Groups were compared to DMSO control using One-way ANOVA, (F(7, 16) = 76.4), followed by Dunnett’s test. P < 0.0001 (****) when compounds were used in normal fibroblasts. P > 0.05 when compounds were used in Tangier fibroblasts: Cpd H, P = 0.4; Cpd J, P > 0.99; T1317, P = 0.5. c Western blot for ABCA1 protein from cholesterol-loaded THP1 macrophages treated with the LXR agonist T1317 or the two ABCA1 inducers, Cpd J and Cpd H. Image representative from three independent experiments. Duplicate protein samples from separate wells were loaded for each treatment. β-Actin was used as a loading control. d Relative mRNA expression level of ABCA1 mRNA determined by quantitative real-time PCR after treatment of cholesterol-loaded THP1 macrophages for 24 h with the indicated compounds and concentrations.