Macrophage ABCA1 and ABCG1, but not SR-BI, promote macrophage reverse cholesterol transport in vivo
J. Clin. Invest. Xun Wang, et al. 117:2216 doi:10.1172/JCI32057 [Go to this article.]

Figure 5
ABCG1-deficient BMMs have reduced cholesterol efflux ex vivo and RCT in vivo. (A) Cholesterol efflux assay was determined as described in Figure 1 with BMMs from WT (ABCG1^+/+) or ABCG1-KO (ABCG1^–/–) mice. Cholesterol efflux was determined in the presence of HDL₃ (25 μg/ml) or lipid-free apoA-I (10 μg/ml) for 2 hours. Data are expressed as mean ± SD; n = 3. *P < 0.05. (B) Cholesterol efflux was determined as described above, except cells were incubated for 2 hours either in the presence or absence probucol (20 μM) prior to the addition of 2.5% mouse whole serum as the acceptor. Data are expressed as mean ± SD; n = 3. **P < 0.01; ***P < 0.001. (C and D) The RCT assay was performed as described in Figure 1 with [³H]cholesterol-labeled, acLDL-loaded, and LXR agonist–treated BMMs from ABCG1^+/+ or ABCG1^–/– mice. n = 8 mice per group. Data are expressed as the percentage of tracer relative to total cpm tracer injected ± SEM. **P < 0.01; ***P < 0.001. Results are representative of 2 independent experiments. (C) Time course of [³H]cholesterol distribution in plasma. Individual time points and areas under the curve were determined and compared. (D) Fecal [³H]tracer levels. Feces were collected continuously from 0 to 48 hours.