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. 2021 Sep 20;30(2):915–931. doi: 10.1016/j.ymthe.2021.09.017

Figure 2.

Figure 2

Knockdown of circCdyl attenuates Ang II-induced AAA formation and decreases the levels of inflammatory molecules associated with M1 macrophages

(A) Images showing the characteristics of aortas from Ang II-infused ApoE−/− mice transfected with circCdyl-knockdown AAV (Sh-circCdyl) or corresponding control AAV (Scr-RNA). (B) Incidence of AAA in Ang II-infused ApoE−/− mice in the two indicated groups. ∗∗p < 0.01; n = 36 per group. (C) Survival curves of Ang II-infused ApoE−/− mice in the two indicated groups. ∗p < 0.05; n = 36 per group. (D) Maximal abdominal aortic outer diameters in Ang II-infused ApoE−/− mice in the two indicated groups. ∗∗p < 0.01; n = 12 per group. (E) EVG staining images and elastin degradation scores in the two indicated groups (scale bars, 200 and 50 μm). ∗∗p < 0.01; n = 12 per group. (F) Plasma concentrations of IL-6, MCP1, and TNF-α from aortas of Ang II-infused ApoE−/− mice in the two indicated groups. ∗∗p < 0.01; n = 5 per group. (G–I) Immunohistochemical staining of Arg1 (G) and iNOS (H) and corresponding densitometric analysis (I) in the aortas of Ang II-infused ApoE−/− mice in the two indicated groups (scale bars, 200 and 50 μm). ∗∗p < 0.05; n = 6 per group. (J) CD206, Arg1, iNOS, MMP9, and CD38 levels in the aortas of Ang II-infused ApoE−/− mice in the two indicated groups (western blot) (β-actin as the internal reference). ∗∗p < 0.01; n = 5 per group.