In vivo quantification of murine aortic cyclic strain, motion, and curvature: Implications for abdominal aortic aneurysm growth

Goergen, Craig J.; Barr, Kyla N.; Huynh, Diem Thi Ngoc; Eastham-Anderson, Jeffrey R.; Choi, Gilwoo; Hedehus, Maj; Dalman, Ronald L.; Connolly, Andrew J.; Taylor, Charles A.; Tsao, Philip S.; Greve, Joan M.

doi:10.1002/jmri.22331

Cited by 55 publications

(66 citation statements)

References 42 publications

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“…Using the AngII apoE −/− mouse model, Goergen et al [50] found a strong correlation between aortic expansion and increased vessel motion and aortic curvature. This is in agreement with their previous findings [108] showing that vessel motion is leftward in the suprarenal aorta where there is large aortic curvature (Figure 3A). Using TOF-MRA, they observed that volumetric expansion increased as cyclic strain decreased in both AngII apoE −/− and elastase AAA mice (Figure 3B) [50].…”

Section: Aortic Diseasesupporting

confidence: 94%

Imaging of Small Animal Peripheral Artery Disease Models: Recent Advancements and Translational Potential

Lin

Phillips

Riggins

et al. 2015

IJMS

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Peripheral artery disease (PAD) is a broad disorder encompassing multiple forms of arterial disease outside of the heart. As such, PAD development is a multifactorial process with a variety of manifestations. For example, aneurysms are pathological expansions of an artery that can lead to rupture, while ischemic atherosclerosis reduces blood flow, increasing the risk of claudication, poor wound healing, limb amputation, and stroke. Current PAD treatment is often ineffective or associated with serious risks, largely because these disorders are commonly undiagnosed or misdiagnosed. Active areas of research are focused on detecting and characterizing deleterious arterial changes at early stages using non-invasive imaging strategies, such as ultrasound, as well as emerging technologies like photoacoustic imaging. Earlier disease detection and characterization could improve interventional strategies, leading to better prognosis in PAD patients. While rodents are being used to investigate PAD pathophysiology, imaging of these animal models has been underutilized. This review focuses on structural and molecular information and disease progression revealed by recent imaging efforts of aortic, cerebral, and peripheral vascular disease models in mice, rats, and rabbits. Effective translation to humans involves better understanding of underlying PAD pathophysiology to develop novel therapeutics and apply non-invasive imaging techniques in the clinic.

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Section: Aortic Diseasesupporting

confidence: 94%

Imaging of Small Animal Peripheral Artery Disease Models: Recent Advancements and Translational Potential

Lin

Phillips

Riggins

et al. 2015

IJMS

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“…Interestingly, however, the aorta of both species exhibits a leftward curvature above the right renal artery, which has been proposed as a determining factor for leftward expansion of AngII AAAs in mice [30,31]. In vivo circumferential cyclic strain is also similar across rats and mice, suggesting there is similar pulsatile loading of the aorta [32].…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II Infusion Does Not Cause Abdominal Aortic Aneurysms in Apolipoprotein E-Deficient Rats

Phillips

Chang²,

Gorman³

et al. 2017

J Vasc Res

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The apolipoprotein E-deficient (apoE^-/-) mouse model has advanced our understanding of cardiovascular disease mechanisms and experimental therapeutics. This spontaneous model recapitulates aspects of human atherosclerosis, and allows for the development of dissecting abdominal aortic aneurysms (AAAs) when combined with angiotensin II. We characterized apoE^-/- rats and hypothesized that, similar to mice, they would develop dissecting AAAs. We created rats with a 16-bp deletion of the apoE gene using transcription activator-like effector nucleases. We imaged the suprarenal aorta for 28 days after implantation of miniosmotic pumps that infuse angiotensin II (AngII, 200 ng/kg/min). Blood pressure (BP), serum lipids and lipoproteins, and histology were also analyzed. These rats did not develop pathological aortic dissection, but we did observe a decrease in circumferential cyclic strain, a rise in BP, and microstructural changes in the aortic medial layer. We also measured increased serum lipids with and without administration of a high-fat diet, but did not detect atherosclerotic plaques. Chronic infusion of AngII did not lead to the formation of dissecting AAAs or atherosclerosis in the rats used in this study. While reduced amounts of atherosclerosis may explain this resistance to dissecting aneurysms, further investigation is needed to fully characterize species-specific differences.

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“…The basis for the suprarenal location of AAAs in mouse models compared with the infrarenal aortic location in humans is undefined. A possible explanation of the difference in AAA locations may be the distinct blood flow characteristics between mice and humans in aneurysm-prone areas of the aorta [32,39,40].…”

Section: Ras In Aaa Modelsmentioning

confidence: 98%

Involvement of the renin–angiotensin system in abdominal and thoracic aortic aneurysms

et al. 2012

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Aortic aneurysms are relatively common maladies that may lead to the devastating consequence of aortic rupture. AAAs (abdominal aortic aneurysms) and TAAs (thoracic aortic aneurysms) are two common forms of aneurysmal diseases in humans that appear to have distinct pathologies and mechanisms. Despite this divergence, there are numerous and consistent demonstrations that overactivation of the RAS (renin-angiotensin system) promotes both AAAs and TAAs in animal models. For example, in mice, both AAAs and TAAs are formed during infusion of AngII (angiotensin II), the major bioactive peptide in the RAS. There are many proposed mechanisms by which the RAS initiates and perpetuates aortic aneurysms, including effects of AngII on a diverse array of cell types and mediators. These experimental findings are complemented in humans by genetic association studies and retrospective analyses of clinical data that generally support a role of the RAS in both AAAs and TAAs. Given the lack of a validated pharmacological therapy for any form of aortic aneurysm, there is a pressing need to determine whether the consistent findings on the role of the RAS in animal models are translatable to humans afflicted with these diseases. The present review compiles the recent literature that has shown the RAS as a critical component in the pathogenesis of aortic aneurysms.

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In vivo quantification of murine aortic cyclic strain, motion, and curvature: Implications for abdominal aortic aneurysm growth

Cited by 55 publications

References 42 publications

Imaging of Small Animal Peripheral Artery Disease Models: Recent Advancements and Translational Potential

Imaging of Small Animal Peripheral Artery Disease Models: Recent Advancements and Translational Potential

Angiotensin II Infusion Does Not Cause Abdominal Aortic Aneurysms in Apolipoprotein E-Deficient Rats

Involvement of the renin–angiotensin system in abdominal and thoracic aortic aneurysms

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