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 5Effects of PPAR-specific ligands on macrophage foam-cell formation in vivo. LDLR
–/– mice were fed a control or HC diet for 4 months and were treated for the last month with PPAR-specific agonists, as indicated. Mice were injected intraperitoneally with thioglycollate after the fourth week of drug treatment and peritoneal macrophages were harvested 4 days later for analysis. (
A) Oil red O staining. Original magnification, ×40. (
B) Quantification of triglycerides and cholesterol. For cholesterol values, total bar height represents total cholesterol. The free cholesterol component is represented by a black bar and esterified cholesterol, calculated as total cholesterol minus free cholesterol, is represented by a white bar. Data are expressed as micrograms per milligram of cell protein and are representative of 2 independent experiments. (
C) Expression of PPARα, β, and γ in normal (white bars) and hypercholesterolemic (black bars) macrophages. Liver is included as a positive control for a tissue expressing relatively high levels of PPARα. (
D) Expression of CD36 mRNA levels determined by real-time PCR. (
E) Expression of ABCA1 and LXRα mRNA levels determined by real-time PCR and Western analysis. Real-time PCR data expressed are mean ± SEM. The results are representative of 2 independent experiments. *
P _ 0.05 versus control, ***
P < 0.001 versus HC control.
