(a) Antisense inhibition of ABC1 reduces cholesterol efflux. Normal human skin fibroblasts were labeled with [³H]cholesterol as described in Methods. Cells were scrape-loaded in the presence of either 30 μM standard control Morpholino oligonucleotide (antisense complement of a β-globin thalassemic mRNA) or 30 μM ABC1 antisense Morpholino oligonucleotide, or were mock-loaded by scraping in the absence of oligonucleotide. Apo A-I–mediated efflux was measured after 12 hours as in the legend to Figure 2. Results presented are the mean ± SEM of 3 separate experiments, normalized to the value for apo A-I–specific efflux in the absence of oligonucleotide in each experiment. (b) Overexpression of ABC1 enhances apo A-I–mediated cholesterol efflux. Parental RAW 264.7 cells and clonal lines 3, 5, and 6 that had been stably transfected with a vector-expressing human ABC1 were cholesterol-loaded and labeled by incubation for 24 hours with 0.5 μCi/mL [³H]cholesterol and 50 μg/mL acetylated LDL, and efflux was measured as described in Methods. Results presented are the mean ± SEM of 3 separate experiments normalized to the value for apo A-I–specific efflux from parental RAW 264.7 cells within each experiment.