Lipid efflux from primary hepatocytes and peritoneal macrophages. Primary mouse hepatocytes were isolated from chow-fed Abca1^+/+ or Abca1^–L/–L mice, stimulated with 9-cis-retanoic acid and 22-OH-cholesterol, and radiolabeled with either [³H]cholesterol or [¹⁴C]choline chloride for 24 hours. After an hour of equilibration, cells were incubated in the presence or absence of 10 μg apoA-I/ml for 24 hours. (A) Hepatocyte cholesterol efflux in the presence or absence of apoA-I. (B) Hepatocyte choline PL efflux in the presence or absence of apoA-I. Data with unlike symbols are significantly different from one another (P < 0.05). (C) Thioglycolate-elicited peritoneal macrophages were isolated from Abca1^+/+ or Abca1^–L/–L mice, radiolabeled with [³H]cholesterol for 24 hours, and then incubated with 10 μM T0901317 or vehicle for an additional 24 hours. Cholesterol efflux was measured after 24-hour incubation of cells, which were stimulated with T0901317 or vehicle in the presence or absence of 20 μg apoA-I/ml. Radiolabel in medium and the cellular isopropanol extract was quantified, and percentage efflux was calculated as the ratio of radioactivity in the medium divided by total radioactivity (cells + media) × 100%. Data are mean ± SD for 3 mice of the indicated genotypes, assayed in triplicate. (D) Western blot of Abca1 or load control protein (GAPDH or β-actin) in cultured hepatocytes (top) or cultured elicited macrophages (bottom).