Differential inhibition of macrophage foam-cell formation and atherosclerosis in mice by PPARα, β/δ, and γ
J. Clin. Invest. Andrew C. Li, et al. 114:1564 doi:10.1172/JCI18730 [Go to this article.]

Figure 4
Determination of scavenger receptor activity and cholesterol efflux in cultured peritoneal macrophages. PPAR-specific agonists, as indicated. (A) Influence of PPAR agonists on uptake (white bars) and degradation (black bars) of oxLDL. (B) Influence of PPAR agonists on CD36 and SRA expression by real-time PCR in hypercholesterolemic macrophages. (C) Influence of LXR and PPAR agonists on apoAI and HDL-specific cholesterol efflux in acLDL-loaded peritoneal macrophages. Expression of LXRα (D) and ABCA1 (E) by real-time PCR in hypercholesterolemic macrophages treated with PPAR agonists in vitro. (F) Western blot analysis of ABCA1 protein in hypercholesterolemic macrophages treated with PPAR agonists as in E. Data are mean ± SEM and are representative of at least 2 independent experiments. In each case, *P _ 0.05, **P _ 0.01, and ***P < 0.001 compared with control. EPC, 24 (S), -25-epoxycholesterol; ¹²⁵I oxLDL, ¹²⁵I-labeled oxLDL.