Fig. 5
Loss of endothelial Prkaa1 increases lesion burden in Apoe−/− mice and accelerates neointima formation. a, b (left) Representative images of Oil Red O stained-aortas (en face) from Apoe−/−/Prkaa1f/f (male n = 13), Apoe−/− Cdh5cre (male n = 8), Apoe−/−/Prkaa1VEC-KO (male n = 21) mice after 16 weeks of Western diet. (Right) Lesion area quantification data. c, d Representative images and quantification data of cross-sections of aortic sinus of Apoe−/−/Prkaa1f/f (n = 5), Apoe−/−/Prkaa1VEC-KO (n = 7) mice with 16 weeks of Western diet. Sections were stained with Oil Red O (lesion), hematoxylin and eosin (plaque), Masson’s trichrome (collagen), and Mac-2 (a macrophage marker). Scale bar: 200 µm. e Representative images of Evans blue staining of injured carotid arteries harvested at the indicated time points in Prkaa1f/f and Prkaa1VEC-KO mice. Scale bar: 500 µm. f Quantification data of percentage of reendothelialization over time in the injured carotid artery from Prkaa1f/f and Prkaa1VEC-KO mice. n = 8, for each time point. g (Left) Representative images of paraffin cross-sections of wire-injured carotid artery from Apoe−/−/Prkaa1f/f (n = 6), Apoe−/−/Prkaa1VEC-KO (n = 7) mice with 4 weeks of Western diet stained with hematoxylin and eosin, Masson’s trichrome, and Mac-2. Scale bar: 100 µm. (Right) Quantification data of lesion size, collagen content, and Mac-2-positive staining. All data were expressed as mean ± SEM. Statistical significance was determined by unpaired Student’s t-test (for d, f, g) and one-way ANOVA followed by Bonferroni test (for b). *p < 0.05 was considered significant, **p < 0.01, ***p < 0.001
