Figure 5.

Expression and activation of LXRα stimulates cholesterol efflux to apoAI through the ABCA1 pathway. (A) Oxysterol ligands of LXR stimulate cholesterol efflux from NIH 3T3 cells. NIH-vector and NIH-LXRα cells were plated in 24-well plates and incubated for 24 h in medium A supplemented with [³H]cholesterol in the absence or presence of the indicated oxysterol (1 μg/ml) or LG268 (LG, 50 nM). ApoAI-dependent cholesterol efflux to the medium was determined as described in Materials and Methods. Data are presented as a percentage (±SE) of the total radioactivity in cells and medium; each point is the numerical average of triplicate experiments. (B) Stimulation of cholesterol efflux by LXR ligands is mediated by ABCA1. Normal or Tangier transformed human skin fibroblasts were plated in 24-well plates and incubated for 24 h in medium A supplemented with [³H]cholesterol in the absence or presence of the indicated oxysterol (1 μg/ml) or LG268 (50 nM). ApoAI-dependent cholesterol efflux to the medium was determined as described in Materials and Methods. Data are presented as a percentage (±SE) of the total radioactivity in cells and medium; each point is the numerical average of triplicate experiments. (Inset) Quantitation of Northern blot analysis of ABCA1 mRNA levels in normal and Tangier fibroblasts normalized for GAPDH expression.