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. 2001 Feb 20;98(5):2610–2615. doi: 10.1073/pnas.041609298

Figure 1.

Figure 1

Area affected by atherosclerotic lesions in the heart outflow tract of apoE −/− mice. (A) Different groups of 15 animals each were treated with a PPARγ agonist, a PPARα/γ coagonist, or a rexinoid. Lesion area was determined as specified in Experimental Procedures. Results are expressed as the mean ± SD. Significance levels (Student's t test) are represented by asterisks (*, P < 0.05; *, *, P < 0.01; *, *, *, P < 0.001). (B) Lesion size as a function of distance to the aortic valves in apoE −/− mice treated as specified in A. Serial sections were cut from the heart valves to the aortic crosses and stained and analyzed as specified. Each point corresponds to the mean surface of lesions measured for the 15 mice in each group at a given distance from the valves. The corresponding standard deviations are not shown, to improve the clarity of the graphic. (C) Representative photographs of atherosclerosis in the aorta of apoE −/− mice, a relevant section from an untreated apoE −/− mouse (control), and an equivalent section of an apoE-deficient mouse after receiving GW2331 (PPARα/γ coagonist) or LG100364 (RXR agonist).