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. 1999 Jun 1;103(11):1597–1604. doi: 10.1172/JCI5897

Figure 3.

Figure 3

12/15-lipoxygenase deficiency results in diminished fatty lesions in apo E-deficient mice. (a) Representative Sudan IV–stained aortas of an apo E–/–/L-12LO–/– double-knockout mouse (left) and an apo E knockout mouse heterozygous for L-12LO (right). Mice were raised on a normal chow diet and sacrificed at 15 weeks of age (n = 12). Atheromatous plaques have already developed in the lesser curvature of the aortic arch (asterisk), at the ostia of the left common carotid artery, and the left subclavian artery (arrow), as well as in the abdominal aorta between the ostia of the left and right renal artery (double asterisk), whereas the aorta of the double-knockout mouse remains free of any lesion development at this age. (b and c) Atherosclerotic average lesion area in en face preparations (n = 12 per group) (b) and aortic sinus areas (n = 12 for L-12LO+/– and L-12LO–/–; n = 9 for L-12LO+/+) (c) in apo E–/– mice lacking L-12LO–/–, expressing 1 allele of L-12LO (L-12LO+/–), or expressing both alleles (L-12LO+/+). Mice fed a normal chow diet were sacrificed at 15 weeks of age. Values are mean ± SEM. **P < 0.0001 (t test). For comparison between groups in c: *P = 0.015 for L-12LO+/+ vs. L-12LO–/– (Mann-Whitney test), P = 0.10 for L-12LO+/– vs. L-12LO–/– (Mann-Whitney test), and P = 0.60 for L-12LO+/+ vs. L-12LO+/– (t test).