Fig. 7. Endothelial S1P₁ suppresses atherosclerotic lesion development.

Male Apoe^−/− S1pr1 WT and Apoe^−/− S1pr1ECKO littermates were placed on high-fat diet for 16 weeks. (A) Aortae were dissected; en face preparation followed by Oil Red O staining was done. Shown here is a representative image of aorta from each group. (B) Quantification of plaque areas in each section of aorta (aortic arch, descending aorta, and total aorta) is shown (six Apoe^−/− WT mice and eight Apoe^−/− S1pr1ECKO mice). ns, not significant. (C) Aortic root sections from Apoe^−/− S1pr1 WT and Apoe^−/− S1pr1ECKO mice were immunostained with MOMA-2 to visualize the infiltration of macrophages and foam cells. (D) Quantification of MOMA-2 infiltration in the aortic valve was assessed (n = 5 mice for each genotype). (E) Plaques from descending aorta of Apoe^−/− S1pr1 WT and Apoe^−/− S1pr1ECKO mice were isolated, and macrophage was visualized by MOMA-2 staining followed by confocal microscopy. (F) Quantification of MOMA-2 staining in the descending aorta lesion was assessed (n = 2 animals, two separate plaques analyzed for each aorta). Data are shown as means ± SD. *P < 0.05, **P < 0.01 by Mann-Whitney test.