Fig. 4

Involvement of Aim2 deficiency in AA formation. a Quantitative analysis of AA incidence in AngII–infused WT mice (n = 31) and Aim2−/− mice (n = 17). Data were analyzed by one-sided Fisher’s exact test. b Representative images of aortas from WT and Aim2−/− mice infused with 1500 ng/kg/min Ang II for 28 days. c, d Total mRNA was extracted from normal aortas or aortic aneurysms of untreated WT (n = 6), untreated Aim2−/− (n = 7), AngII-infused WT (n = 3) and AngII-infused Aim2−/− (n = 3) mice. c Expression of Cdkn2a mRNA is increased in aortas from Aim2−/− mice d Acta 2 mRNA is increased in aortas from AngII infused WT mice. e Western blot, demonstrating increased expression of p16ink4A in aortic lysates of untreated Aim2−/− mice. f Increased mRNA expression of Cdkn2a (p16) and reduced mRNA expression of Acta2 was detected in AA compared with non-AA from AngII infused animals. Bars show the mean ± SEM. c, d, f Data were tested by one-way ANOVA. ns: not significant, *: P < 0.05, **: P < 0.01, ***: P < 0.001. g Aortic sections immunohistochemically stained for α-SMA and p16ink4A