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. Author manuscript; available in PMC: 2019 Dec 1.
Published in final edited form as: J Vasc Surg. 2018 Apr 21;68(6 Suppl):48S–59S.e1. doi: 10.1016/j.jvs.2017.11.091

Fig 4.

Fig 4.

Angiotensin II (Ang II)-induced aneurysm development was suppressed by receptor activator of nuclear factor κB ligand (RANKL)-neutralizing antibody. RANKL (5 mg/kg)-neutralizing antibody was subcutaneously administered to apoE−/− mice. After 7 days, Ang II (1000 ng/min/kg) was continuously infused by an osmotic pump. The maximum diameter of the abdominal aortas was measured to evaluate the severity of aneurysm formation. A, Images of Ang II-induced dissecting abdominal aortic aneurysm (Ang II-induced AAA). B, Images of Ang II-induced AAA after administration of RANKL-neutralizing antibody. C, Maximum diameter of abdominal aortas in response to RANKL-neutralizing antibody (n = 4). Anti-RANKL antibody significantly suppressed Ang II-induced AAA formation. D, Representative images of tartrate-resistant acid phosphatase (TRAP)-positive staining of Ang-II induced AAA tissues. Anti-RANKL antibody suppressed TRAP-positive staining. Scale bar = 0.5 mm. E, Representative Western blot and densitometry analysis of matrix metalloproteinase 9 (MMP9) expression in aortas. Anti-RANKL antibody significantly suppressed MMP9 expression. Values are means ± standard deviations of three replicates.

*P < .05. Relative expression was quantified in Western blots using ImageJ.