Fig. 7: Effects of CCL3 on CaCl2-induced AAA formation in WT, Ccl3−/−, or Ccr5−/− mice.
a, g, m Aortic diameters before and after CaCl2 treatment (n = 6 each in all groups). **P < 0.01, *P < 0.05, vs. pretreatment in each strain; ##P < 0.01, CCL3 vs. PBS treatment. b, h, n Histopathological analysis of the aortas obtained from WT, Ccl3−/−, and Ccr5−/− mice after CaCl2 treatment. Representative results from five independent experiments are shown here. Scale bars, 100 μm. c, i, o Quantification of the number of elastin breaks per vessel (n = 5 each in all groups). *P < 0.05, **P < 0.01, vs. PBS. d, j, p The effects of CCL3 on macrophage accumulation into aortic tissues after CaCl2 treatment. Representative results from six independent experiments are shown. Scale bars, 50 μm. e, k, q Macrophage numbers were measured. (e, q: n = 6 samples in all groups; k: n = 5 samples in all groups). **P < 0.01, *P < 0.05, vs. PBS-treated mice. f, l, r Intra-aortic Mmp9 expression in CaCl2-treated WT, Ccl3−/− or Ccr5−/− mice after CCL3 treatment (n = 6 samples in all groups). **P < 0.01, vs. PBS-treated mice. Unpaired two-sided Student’s t test was used in (a), (c–f), (g), (i–l), (m), and (o–r). Data are presented as mean values ± SEM.
