Alterations in Angiotensin Converting Enzyme During Rodent Aortic Aneurysm Formation

Eagleton, Matthew J.; Cho, Brenda; Lynch, Erin M.; Roelofs, Karen J.; Woodrum, Derek T.; Stanley, James C.; Upchurch, Gilbert R.

doi:10.1016/j.jss.2005.09.023

Cited by 5 publications

(4 citation statements)

References 20 publications

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“…Without the availability of a highly specific antimurine Ang II or AT1a antibody, neither aortic AT1a nor aortic or serum Ang II expression or circulating levels could be quantified during or after aneurysm creation in this modeling system. At least one prior study has reported transient increases in aortic mRNA expression levels of ACE, an enzyme responsible for converting Ang I to Ang II, after intra-aortic PPE infusion, 36 providing at least indirect evidence that endogenous Ang II levels are indeed elevated in this model. Some ARBs also block the “b” subtype of AT1, 37,38 raising the possibility that AT1b inhibition may contribute to some of the observed inhibitory effects of telmisartan.…”

Section: Discussionmentioning

confidence: 75%

Inhibition or deletion of angiotensin II type 1 receptor suppresses elastase-induced experimental abdominal aortic aneurysms

Xuan

Wang

et al. 2018

Journal of Vascular Surgery

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Section: Discussionmentioning

confidence: 75%

Inhibition or deletion of angiotensin II type 1 receptor suppresses elastase-induced experimental abdominal aortic aneurysms

Xuan

Wang

et al. 2018

Journal of Vascular Surgery

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“…129 In a rabbit model for aneurysm formation (elastase perfusion), aortic wall ACE protein levels increased during aneurysm growth in time. 130 In mice, infusion of Ang II induced aneurysm formation independent of blood pressure changes. This was shown in a hyperlipidemic setting (in ApoE Ϫ/Ϫ mice) and in wild-type C57BL6 mice, although aneurysm formation was smaller in the wild-type mice.…”

Section: Ace and Aneurysm Formationmentioning

confidence: 99%

Angiotensin-Converting Enzyme and Vascular Remodeling

Heeneman

Sluimer

Daemen

2007

Circulation Research

187

132

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Abstract-Vascular remodeling is the result of a close interplay of changes in vascular tone and structure. In this review, the role of angiotension-converting enzyme (ACE) and the impact of ACE inhibition on vascular remodeling processes during vascular injury and restenosis, hypertension, atherosclerosis, and aneurysm formation are discussed. The role of ACE and angiotensin II (Ang II) in neointimal thickening has been firmly established by animal studies and is mediated by Ang II type 1 (AT 1 ) receptor signaling events via monocyte chemoattractant protein-1 and NAD(P)H oxidase. ACE and Ang II are involved in the remodeling of large and resistance arteries during hypertension; here, cell proliferation and matrix remodeling are also regulated by signaling events downstream of the AT 1 receptor. In atherosclerosis, Ang II is involved in the inflammatory and tissue response, mediated by various signaling pathways downstream of the AT 1 receptor. Although ACE inhibition has been shown to inhibit atherosclerotic processes in experimental animal models, results of large clinical trials with ACE inhibitors were not conclusive. Remodeling of vessel dimensions and structure during aneurysm formation is counteracted by ACE inhibition. Here, a direct effect of ACE inhibitors on matrix metalloproteinase activity has to be considered as part of the working mechanism. The role of ACE2 in vascular remodeling has yet to be established; however, ACE2 has been shown to be associated with vascular changes in hypertension and atherosclerosis. (Circ Res. 2007;101:441-454.)

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“…In elastaseapplied aorta in rats, both ACE gene expression and protein levels were augmented along with the expansion of the aorta after elastase application (33). Angiotensin II is known to induce MMP9 gene expres sion via augmentation of ROS, and the augmentation of MMP9 may play a critical role in the pathogenesis of AAA induced by elastase in mice (7,8,31,34).…”

Section: Discussionmentioning

confidence: 99%

Significance of Matrix Metalloproteinase-9 Inhibition by Imidapril for Prevention of Abdominal Aortic Aneurysms in Angiotensin II Type 1 Receptor–Knockout Mice

Jin

Yamamoto

et al. 2013

J Pharmacol Sci

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To clarify the matrix metalloproteinase (MMP)-9 inhibitory effect of an angiotensin-converting enzyme (ACE) inhibitor in vivo, we evaluated the effect of an ACE inhibitor against elastase-induced abdominal aortic aneurysm (AAA) progression in mice. Molecular models showed that imidapril bound directly to the mouse MMP-9 active center. An active form of imidapril, imidaprilat, dose-dependently inhibited MMP-9 activity in the extract from elastase-induced AAA in wild-type mice. Imidapril (10 mg/kg per day) was administered to wild-type or angiotensin II type 1 (AT1) receptor knockout mice. Blood pressure was significantly lower in AT1 receptor-knockout mice than in wild-type mice, but imidapril did not affect blood pressure in AT1 receptor-knockout mice. The aortic diameter was significantly expanded after elastase application, but the expansion was significantly lower in AT1 receptor-knockout mice than in wild-type mice. In AT1 receptor-knockout mice, the aortic expansion was further attenuated by imidapril. MMP-9 activity in aorta was significantly augmented after elastase application. The MMP-9 activity was significantly lower in AT1 receptor-knockout mice than in wild-type mice, and it was further attenuated by imidapril. In conclusion, MMP-9 inhibition by imidapril might contribute to the attenuation of AAA progression in AT1 receptor-knockout mice.

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Alterations in Angiotensin Converting Enzyme During Rodent Aortic Aneurysm Formation

Cited by 5 publications

References 20 publications

Inhibition or deletion of angiotensin II type 1 receptor suppresses elastase-induced experimental abdominal aortic aneurysms

Inhibition or deletion of angiotensin II type 1 receptor suppresses elastase-induced experimental abdominal aortic aneurysms

Angiotensin-Converting Enzyme and Vascular Remodeling

Significance of Matrix Metalloproteinase-9 Inhibition by Imidapril for Prevention of Abdominal Aortic Aneurysms in Angiotensin II Type 1 Receptor–Knockout Mice

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