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. 2011 Feb;52(2):345–353. doi: 10.1194/jlr.M012328

Fig. 2.

Fig. 2.

ABCG1-mediated cholesterol efflux to nascent HDL particles. Transfected BHK cells were labeled with [3H] cholesterol and then induced to express ABCG1 as described in “Materials and Methods.” Cellular cholesterol efflux stimulated by 5 h incubations with either lipid-poor apoA-I or SAA or conditioned media from THP-1 cells incubated with apoA-I or SAA (10 µg/ml apolipoprotein) was determined. ABCG1-dependent efflux represents the difference between BHK cells treated with mifepristone (Total) and untreated cells (ABCG1-independent). Values are the mean ± SEM of triplicate determinations. Total and ABCG1-independent efflux to lipid-poor apoA-I and SAA, or THP-1-conditioned apoA-I and SAA data were analyzed using one way ANOVA with Tukey-adjusted pairwise comparisons. Different lower case letters identify different means among apoA-I groups; different capital letters identify different means among SAA groups (P ≤ 0.004). In addition, the ABCG1-dependent component was compared across groups in posthoc tests. ★★★ indicates P < 0.001. Similar results were obtained in two additional experiments. ABCG1, ATP binding cassette transporter G1; apoA-I, apolipoprotein A-I; BHK, baby hamster kidney; SAA, serum amyloid A.