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. 2019 Mar 12;19(5):3459–3468. doi: 10.3892/mmr.2019.10017

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Copyright: © Sun et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 1. — AAA is induced by Ang II in ApoE^−/− mice. (A) Morphology of Ang II-induced AAA and normal aortas (control) in ApoE^−/− mice; white arrows indicate a typical AAA. (B) Aorta cross-sections stained with hematoxylin and eosin. (C) Representative immunofluorescence and TUNEL staining for the detection of DNA fragmentation in Ang II-induced AAA and saline-treated aortas (magnification, ×200). (D) TUNEL assay for detecting cell apoptosis in MOVAS cells treated (or not treated, saline) with Ang II by fluorescence microscopy (magnification, ×400). Light green indicates normal DNA (TUNEL-) and bright green indicates damaged DNA (TUNEL+). **P<0.01 vs. respective Sham. AAA, abdominal aortic aneurysm; Ang II, angiotensin II; ApoE^−/−, apolipoprotein E-deficient; TUNEL, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling; α-SMA, α-smooth muscle actin.