Effect of the carboxyl-terminal deletion mutant apoA-I[Δ(185–243)] bound to rHDL particles on ABCG1-mediated 7-ketocholesterol efflux from HEK293 cells transfected with an ABCG1-expressing plasmid and from J774 mouse macrophages following treatment with AICAR.

<p>(A) HEK293 cells were transfected with empty vector (mock) or with ABCG1 plasmid, labeled with [³H]7-ketocholesterol for 24 h and then incubated with rHDL containing WT apoA-I or apoA-I[Δ(185–243)], at a concentration of 1 µM apoA-I, for 4 h. (B, C) J774 mouse macrophages were labeled with [³H]7-ketocholesterol (B) or [³H]7-ketocholesterol and 30 µg/ml acLDL (C) for 24 h and then incubated with 1 mM AICAR for 24 h. At the end of this incubation period the cells were incubated with rHDL containing WT apoA-I or apoA-I[Δ(185–243)], at a concentration of 1 µM apoA-I, for 4 h. The net ABCG1-mediated [³H]7-ketocholesterol efflux is calculated as the difference in percent of 7-ketocholesterol efflux between ABCG1-transfected and mock-transfected cells (A) or between untreated and AICAR-treated cells (B, C). Values are the means ± SD from three independent experiments performed in duplicate.