Fig. 5: The roles of CCL3 receptors in CaCl₂-induced AAA formation.

a Aortic diameters in WT, Ccr1^−/−, and Ccr5^−/− mice after CaCl₂ treatment. (Pre: n = 6 in each strain; 6 week- n = 7 each in WT and Ccr1^−/−, n = 8 in Ccr5^−/−). **P < 0.01, vs. pretreatment; ^##P < 0.01, vs. WT mice. b Histopathological analysis of the aortas obtained from WT, Ccr1^−/−, and Ccr5^−/− mice after CaCl₂ treatment. Representative results from four independent experiments are shown here. Scale bar = 100 µm. c Quantification of the number of elastin breaks per vessel (n = 5 in each mouse strain). **P < 0.01, vs. WT mice. d Macrophage accumulation into aortic tissues of WT, Ccr1^−/−, and Ccr5^−/− mice after CaCl₂ treatment. Representative results from five independent experiments are shown. Scale bar, 50 µm. e Macrophage numbers were measured (n = 5 in each mouse strain). **P < 0.01, vs. WT mice. f Intra-aortic Mmp9 expression in WT, Ccr1^−/−, and Ccr5^−/− mice after CaCl₂ treatment (n = 6 in each mouse strain). **P < 0.01, vs. pretreatment in each strain. g Aortic diameters in CaCl₂-treated mice after maraviroc application (n = 4 each). **P < 0.01, vs. pretreatment in each group; ^#P < 0.05, vehicle-treated WT vs. vehicle-treated Ccl3^−/−WT mice; ^§P < 0.05, maraviroc-treated WT vs. vehicle-treated WT. h CCR5-expressing cells in aortic tissues of WT mice after CaCl₂ treatment. Representative results from four independent experiments are shown. Scale bar = 40 µm. Blue, nuclear staining by DAPI. i Aortic diameters in CaCl₂-treated mice after an MMP-9 inhibitor application (n = 5 in vehicle-6 week for WT, n = 4 each in other all groups). **P < 0.01, vs. pretreatment in each group; ^##P < 0.01, vs. vehicle-treated mice of each strain. Unpaired two-sided Student’s t test was used in (a), (c), (e), (f), (g), and (i). Data are presented as mean values ± SEM.