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 1
ABCA1-deficient BMMs have reduced cholesterol efflux ex vivo and RCT in vivo. (A) BMMs from WT (ABCA1^+/+) or ABCA1-KO (ABCA1^–/–) mice were labeled with [³H]cholesterol and loaded with 25 μg/ml acLDL for 24 hours. Cells were equilibrated for 18 hours in the presence of 1 μM LXR agonist (GW3965). Then, cells were incubated for 2 hours in either the presence of absence of probucol (20 μM). Cholesterol efflux was determined in the presence of lipid-free apoA-I (10 μg/ml) for 2 hours. Data are expressed as mean ± SD; n = 3. ***P < 0.001. (B) Cholesterol efflux was determined as described above, except 2.5% mouse whole serum was used as the acceptor. Data are expressed as mean ± SD; n = 3. ***P < 0.001. (C and D) For the in vivo RCT experiment, WT C57BL/6 mice that had been treated with an LXR agonist for 2 weeks were injected i.p. with [³H]cholesterol-labeled, acLDL-loaded, and LXR agonist–treated BMMs from ABCA1^+/+ or ABCA1^–/– mice. Mice were bled at 2, 6, 24, and 48 hours after injection. n = 8 mice per group. Data are expressed as the percentage of tracer relative to total cpm tracer injected ± SEM. **P < 0.01. 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.