scholarly journals The murine angiotensin II-induced abdominal aortic aneurysm model: rupture risk and inflammatory progression patterns

2010 ◽  
Author(s):  
Richard Y. Cao
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Angiotensin Ii ◽  
Aortic Aneurysm ◽  
Rupture Risk ◽  
Abdominal Aortic ◽  
Aneurysm Model ◽  
Progression Patterns

scholarly journals Long-Term Effects of the Abdominal Aortic Aneurysm Model in Rabbits Prepared by Pancreatic Elastase Combined With Angiotensin II

2018 ◽  
Vol 53 (1) ◽  
pp. 35-41
Author(s):  
Qing Chen ◽  
Mao-xiao Nie ◽  
Quan-ming Zhao
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Angiotensin Ii ◽  
Aortic Aneurysm ◽  
Pancreatic Elastase ◽  
Aneurysm Formation ◽  
Abdominal Aortic ◽  
Group A ◽  
Aneurysm Diameter ◽  
Aneurysm Model

Objective: This study aimed to observe the effect of pancreatic elastase combined with angiotensin II on a stable rabbit abdominal aortic aneurysm model. Methods: A total of 20 male New Zealand rabbits were randomly divided into groups A and B, with 10 rabbits per group. The rabbits in group A were given an intraperitoneal perfusion of pancreatic elastase, and the rabbits in group B were given continuous pumping of angiotensin II in addition to the operation of group A. Before the operation and at 2, 4, and 16 weeks postoperation, vascular color Doppler ultrasonography was performed, and blood samples were collected to measure the serum matrix metalloproteinase 9 (MMP9) and MMP2 levels. At 16 weeks postoperation, all rabbits in both groups were killed, and hematoxylin and eosin, Elastic-van-Gieson, Masson’s, and immunohistochemical staining were performed for the vessel specimens. Results: At 2 weeks postoperation, the aneurysm formation rates of the 2 groups were both 100%, and the average expansion rates of the aneurysm diameters were 85% and 93%, respectively; these differences were not significant ( P = .150 and P = .280, respectively). At 4 weeks postoperation, the aneurysm formation rates of the 2 groups were 71.4% and 100%, and the average expansion rates of the aneurysm diameter were 68% and 99%, respectively; the differences between the groups were significant ( P = .031 and P = .022, respectively). At 16 weeks postoperation, the aneurysm formation rates of the 2 groups were 14.3% and 100%, and the average expansion rates of the aneurysm diameter were 12% and 108%, respectively; the differences between the groups were significant ( P = .026 and P = .014, respectively). Conclusion: Compared to the abdominal aortic aneurysm modeling method in rabbits based on pancreatic elastase alone, the abdominal aortic aneurysm modeling method in rabbits using pancreatic elastase combined with angiotensin II maintained the morphology of the abdominal aortic aneurysm for a longer time, showing an important application value for the long-term observation of changes in abdominal aortic aneurysms.

scholarly journals Endothelial Cell Tetrahydrobiopterin Modulates Sensitivity to Ang (Angiotensin) II–Induced Vascular Remodeling, Blood Pressure, and Abdominal Aortic Aneurysm

Hypertension ◽  
2018 ◽  
Vol 72 (1) ◽  
pp. 128-138 ◽  
Author(s):  
Surawee Chuaiphichai ◽  
Victoria S. Rashbrook ◽  
Ashley B. Hale ◽  
Lucy Trelfa ◽  
Jyoti Patel ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Abdominal Aortic Aneurysm ◽  
Endothelial Cell ◽  
Angiotensin Ii ◽  
Aortic Aneurysm ◽  
Vascular Remodeling ◽  
Abdominal Aortic

Abstract 279: Role of Caveolin-1 in Abdominal Aortic Aneurysm induced by Angiotensin II

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Takehiko Takayanagi ◽  
Kevin Crawford ◽  
Tomonori Kobayashi ◽  
Victor Rizzo ◽  
Satoru Eguchi
Keyword(s):  
Oxidative Stress ◽  
Abdominal Aortic Aneurysm ◽  
Angiotensin Ii ◽  
Aortic Aneurysm ◽  
Egf Receptor ◽  
Critical Role ◽  
Membrane Microdomains ◽  
Structural Protein ◽  
Caveolin 1 ◽  
Abdominal Aortic

Abdominal aortic aneurysm (AAA) is a significant cause of mortality for adults aged >60 years. Accumulating evidence suggests that activation of the AT1 receptor by angiotensin II (AngII) in AAA formation. While several downstream signals and target proteins have been identified in this pathway, there is a huge void in our knowledge regarding the AngII-sensitive proximal events primarily responsible for AAA formation. We recently reported that caveolae membrane microdomains in vascular smooth muscle cells (VSMC) mediate a metalloprotease ADAM17-dependent EGF receptor (EGFR) transactivation which linked to vascular remodeling induced by AngII. Given that ADAM17 expression is one of the key features in AAA, we have tested our hypothesis that caveolin-1 (Cav1), a major structural protein of caveolae, in the vasculature plays a critical role for development of AAA via its regulation on ADAM17. 8 week old male Cav1-/- mice and the control C57Bl/6 wild-type (WT) mice were co-infused with AngII and BAPN, a lysyl oxidase inhibitor, to induce AAA. We found that Cav1-/- mice did not develop AAA compared to C57Bl/6 mice in spite of hypertension assessed by telemetry in both groups. This finding suggests that the AngII signaling essential for vascular contraction remains in place in Cav1-/- mice. We found an increased expression of ADAM17 and auto-phosphorylation of EGFR in WT abdominal aortae with aneurysms that were markedly attenuated in Cav1-/- mice infused with AngII+BAPN. Furthermore, Cav1-/- mice with the infusion showed less oxidative stress and ER stress than their WT counterparts as assessed by nitrotyrosine staining and KDEL/p-eIF2a staining, respectively. In conclusion, Cav1 and presumably vascular caveolae micro-domain appear to play a critical role in the formation of AAA in mice via regulation of the ADAM17/EGFR signaling axis and subsequent induction of ER/oxidative stress.

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