The efficacy of apolipoprotein E deficiency in cerebral aneurysm formation

Aoki, Tomohiro; Moriwaki, Takuya; Takagi, Yasushi; Kataoka, Hiroharu; Yang, Jin‐Long; Nozaki, Kazuhiko; Hashimoto, Nobuo

doi:10.3892/ijmm.21.4.453

Cited by 10 publications

(14 citation statements)

References 19 publications

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“…Further, 16% of C57BL/6 wild‐type mice developed advanced intracranial aneurysms compared to 17% of ApoE −/− mice. Similarly, 32% of wild‐type mice developed early aneurysmal changes compared to 28% of ApoE −/− mice . This was in agreement with a clinical report which showed that ApoE alleles were not associated with the incidence of intracranial aneurysm .…”

Section: The Molecular Mechanisms Involved In Intracranial Aneurysm Dsupporting

confidence: 90%

“…Twenty‐two publications that report the use of mouse models of intracranial aneurysm were identified by searching the PubMed database . In these papers, five mouse models of intact intracranial aneurysm (see the following sections) and two mouse models of ruptured intracranial aneurysm (see the following sections) have been reported (Table ).…”

Section: Mouse Models Of Intracranial Aneurysmmentioning

confidence: 99%

“…Another 10 studies used light microscopy of arterial sections to define intracranial aneurysms as an outward bulging of the arterial wall with fragmentation or disappearance of the internal elastic lamina . In these studies, histological assessments were performed with a variety of techniques including orcein or Elastica van Gieson staining methods.…”

Section: Definitions Of Intracranial Aneurysm Used In Previous Mouse mentioning

confidence: 99%

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Mouse Models of Intracranial Aneurysm

et al. 2014

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Subarachnoid hemorrhage secondary to rupture of an intracranial aneurysm is a highly lethal medical condition. Current management strategies for unruptured intracranial aneurysms involve radiological surveillance and neurosurgical or endovascular interventions. There is no pharmacological treatment available to decrease the risk of aneurysm rupture and subsequent subarachnoid hemorrhage. There is growing interest in the pathogenesis of intracranial aneurysm focused on the development of drug therapies to decrease the incidence of aneurysm rupture. The study of rodent models of intracranial aneurysms has the potential to improve our understanding of intracranial aneurysm development and progression. This review summarizes current mouse models of intact and ruptured intracranial aneurysms and discusses the relevance of these models to human intracranial aneurysms. The article also reviews the importance of these models in investigating the molecular mechanisms involved in the disease. Finally, potential pharmaceutical targets for intracranial aneurysm suggested by previous studies are discussed. Examples of potential drug targets include matrix metalloproteinases, stromal cell-derived factor-1, tumor necrosis factor-α, the renin-angiotensin system and the β-estrogen receptor. An agreed clear, precise and reproducible definition of what constitutes an aneurysm in the models would assist in their use to better understand the pathology of intracranial aneurysm and applying findings to patients.

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Section: The Molecular Mechanisms Involved In Intracranial Aneurysm Dsupporting

confidence: 90%

Section: Mouse Models Of Intracranial Aneurysmmentioning

confidence: 99%

Section: Definitions Of Intracranial Aneurysm Used In Previous Mouse mentioning

confidence: 99%

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Mouse Models of Intracranial Aneurysm

et al. 2014

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“…In pathological studies, CA is not accompanied by atherosclerosis (26). Furthermore, in ApoE knockout mice, which presented marked hypercholesterolemia, CA formation was not changed, indicating that hypercholesterolemia, a main risk factor of atherosclerosis, might not be responsible for CA formation (27). MMP-9 is a proteinase with both collagenase and elastase activity, and plays a critical role in both CA (25) and AAA formation (28,29).…”

Section: Discussionmentioning

confidence: 99%

Role of angiotensin II type 1 receptor in cerebral aneurysm formation in rats

Aoki

Nakagawa²,

Kataoka³

et al. 2009

Int J Mol Med

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Abstract. Cerebral aneurysm (CA) causes catastrophic subarachnoid hemorrhage which is characterized by a high mortality and morbidity rate. CA is a common disease worldwide but to date there is no medical treatment against unruptured CAs. Thus, it is important to study the mechanisms of CA formation. Our previous report demonstrated that chronic inflammatory response in cerebral arterial bifurcation by hemodynamic stress deteriorated arterial walls and formed CA. Therefore, drugs with anti-inflammatory effects might effectively treat CA formation. As renin angiotensin system (RAS) is a major inflammatory cascade and related to various vascular diseases, including aortic aneurysms, the role of angiotensin (Ang) II type 1 receptor might contribute to the progression of CAs. However, in cerebral aneurysmal walls, Ang II type 1 receptor was not up-regulated. In addition, subcutaneously administered Ang II type 1 receptor blocker did not inhibit CA formation, nor inflammation in cerebral aneurysmal walls in rat models at a sub-suppressor dose. These results indicate that RAS might play a less important role in CA formation compared to aortic anuerysms or other vascular diseases. This suggests that there are different mechanisms between the pathogenesis of cereberal and aortic aneurysms.

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“…In the pathogenesis of aneurysm formation, there are similarities and differences between abdominal aortic aneurysm (AAA) and cerebral aneurysm (CA). AAAs are shown to initiate and progress from arteriosclerotic changes, but there are no apparent arteriosclerotic changes in saccular aneurysm walls2). However, the fusiform and giant CA have different underlying pathologies, hemodynamics, anatomical distributions and natural histories when compared to the saccular CA15).…”

Section: Introductionmentioning

confidence: 99%

Dysregulated Expression Profiles of MicroRNAs of Experimentally Induced Cerebral Aneurysms in Rats

Lee

et al. 2013

J Korean Neurosurg Soc

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ObjectiveCerebral aneurysm (CA) is an important acquired cerebrovascular disease that can cause catastrophic results. MicroRNAs (miRNAs) are small non-coding RNAs, playing essential roles in modulating basic physiologic and pathological processes. Currently, evidences have been established about biologic relationship between miRNAs and abdominal aortic aneurysms. However, biologic roles of miRNAs in CA formation have not been explained yet. We employed microarray analysis to detect and compare miRNA expression profiles in late stage of CA in rat model.MethodsTwenty-six, 7-week-old male Sprague-Dawley rats underwent a CA induction procedure. The control animals (n=11) were fed a normal diet, and the experimental animals (n=26) were fed a normal diet with 1% normal saline for 3 months. Then, the rats were sacrificed, their cerebral arteries were dissected, and the five regions of aneurysmal dilation on the left posterior communicating artery were cut for miRNA microarrays analysis. Six miRNAs (miRNA-1, miRNA-223, miRNA-24-1-5p, miRNA-551b, miRNA-433, and miRNA-489) were randomly chosen for validation using real-time quantitative PCR.ResultsAmong a set of differentially expressed miRNAs, 14 miRNAs were over-expressed more than 200% and 6 miRNAs were down-expressed lower than 50% in the CA tissues.ConclusionThe results show that miRNAs might take part in CA formation probably by affecting multiple target genes and signaling pathways. Further investigations to identify the exact roles of these miRNAs in CA formation are required.

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The efficacy of apolipoprotein E deficiency in cerebral aneurysm formation

Cited by 10 publications

References 19 publications

Mouse Models of Intracranial Aneurysm

Mouse Models of Intracranial Aneurysm

Role of angiotensin II type 1 receptor in cerebral aneurysm formation in rats

Dysregulated Expression Profiles of MicroRNAs of Experimentally Induced Cerebral Aneurysms in Rats

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