scholarly journals Murine ultrasound imaging for circumferential strain analyses in the angiotensin II abdominal aortic aneurysm model

2012 ◽  
Vol 56 (2) ◽  
pp. 462-469 ◽  
Author(s):  
John T. Favreau ◽  
Binh T. Nguyen ◽  
Ian Gao ◽  
Peng Yu ◽  
Ming Tao ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Angiotensin Ii ◽  
Aortic Aneurysm ◽  
Ultrasound Imaging ◽  
Circumferential Strain ◽  
Abdominal Aortic ◽  
Aneurysm Model

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.

scholarly journals Comparison of Abdominal Aortic Aneurysm Sac and Neck Wall Motion with 4D Ultrasound Imaging

2020 ◽  
Vol 60 (4) ◽  
pp. 539-547
Author(s):  
Wojciech Derwich ◽  
Andreas Wittek ◽  
Achim Hegner ◽  
Claus-Peter Fritzen ◽  
Christopher Blase ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Ultrasound Imaging ◽  
Wall Motion ◽  
4D Ultrasound ◽  
Abdominal Aortic

scholarly journals IKK Epsilon Deficiency Attenuates Angiotensin II-Induced Abdominal Aortic Aneurysm Formation in Mice by Inhibiting Inflammation, Oxidative Stress, and Apoptosis

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Hao Chai ◽  
ZhongHao Tao ◽  
YongChao Qi ◽  
HaoYu Qi ◽  
Wen Chen ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Angiotensin Ii ◽  
Aortic Aneurysm ◽  
Molecular Mechanisms ◽  
Critical Role ◽  
Ang Ii ◽  
Elastin Degradation ◽  
Maximal Diameter ◽  
Abdominal Aortic ◽  
Primary Mouse

Abdominal aortic aneurysm (AAA) is a vascular disorder that is considered a chronic inflammatory disease. However, the precise molecular mechanisms involved in AAA have not been fully elucidated. Recently, significant progress has been made in understanding the function and mechanism of action of inhibitor of kappa B kinase epsilon (IKKε) in inflammatory and metabolic diseases. The angiotensin II- (Ang II-) induced or pharmacological inhibitors were established to test the effects of IKKε on AAA in vivo. After mice were continuously stimulated with Ang II for 28 days, morphologically, we found that knockout of IKKε reduced AAA formation and drastically reduced maximal diameter and severity. We also observed a decrease in elastin degradation and medial destruction, which were independent of systolic blood pressure or plasma cholesterol concentrations. Western blot analyses and immunohistochemical staining were carried out to measure IKKε expression in AAA tissues and cell lines. AAA phenotype of mice was measured by ultrasound and biochemical indexes. In zymography, immunohistology staining, immunofluorescence staining, and reactive oxygen species (ROS) analysis, TUNEL assay was used to examine the effects of IKKε on AAA progression in AAA mice. IKKε deficiency significantly inhibited inflammatory macrophage infiltration, matrix metalloproteinase (MMP) activity, ROS production, and vascular smooth muscle cell (VSMC) apoptosis. We used primary mouse aortic VSMC isolated from apolipoprotein E (Apoe) −/− and Apoe−/−IKKε−/− mice. Mechanistically, IKKε deficiency blunted the activation of the ERK1/2 pathway. The IKKε inhibitor, amlexanox, has the same impact in AAA. Our results demonstrate a critical role of IKKε in AAA formation induced by Ang II in Apoe−/− mice. Targeting IKKε may constitute a novel therapeutic strategy to prevent AAA progression.

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