Fig. 9: The roles of the CCL3–CCR5 axis on Ang II-induced AAA formation.

a Systolic blood pressure at the indicate time points after Ang II infusion (Pre: n = 7 in each mouse strain; 2 week: n = 9 in WT mice, n = 4 each in Ccl3^−/− and Ccr1^−/−, n = 5 in Ccr5^−/− mice; 4 week: n = 4 each in WT, Ccr1^−/−, and Ccr5^−/−mice, n = 5 in Ccl3^−/− mice). b Representative macroscopic appearance of the aorta in each mouse strain after Ang II infusion. c The diameters of the aorta in mice at 4 weeks after Ang II infusion (Pre: n = 6 each in WT and Ccl3^−/− mice, n = 5 each in Ccr1^−/− and Ccr5^−/−mice; 4 week: n = 12 each in WT and Ccr5^−/−mice, n = 14 in Ccl3^−/− mice, n = 10 in Ccr1^−/− mice). **P < 0.01, *P < 0.05, vs. posttreatment in WT mice. d Incidence of AAA in WT, Ccl3^−/−, Ccr1^−/−, and Ccr5^−/− mice after Ang II infusion. *P < 0.05, vs. WT. e Histopathological analysis of the aortas obtained from WT, Ccl3^−/−, Ccr1^−/−, and Ccr5^−/− mice after Ang II application^. f Intra-aortic MMP-9 activities were measured by gelatin zymography on day 5 after Ang II infusion. M molecular weight marker. 1 and 5, WT; 2 and 6, Ccl3^−/−; 3 and 7, Ccr1^−/−; 4 and 8, Ccr5^−/−. Independent experiments were repeated four times. Unpaired two-sided Student’s t test was used in (a) Steel–Dwass’s multiple comparison test was used in (d). Data are presented as mean values ± SEM.