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诱导小鼠肌内膜增生与动脉粥样硬化:两种有效模型介绍

Inducing myointimal hyperplasia versus atherosclerosis in mice: an introduction of two valid models.

作者信息

Stubbendorff Mandy, Hua Xiaoqin, Deuse Tobias, Ali Ziad, Reichenspurner Hermann, Maegdefessel Lars, Robbins Robert C, Schrepfer Sonja

机构信息

Transplant and Stem Cell Immunobiology Lab, Cardiovascular Research Center, University Hospital Hamburg; Cardiovascular Research Center (CVRC) and DZHK University Hamburg.

Transplant and Stem Cell Immunobiology Lab, Cardiovascular Research Center, University Hospital Hamburg; Cardiovascular Research Center (CVRC) and DZHK University Hamburg; Department of Cardiovascular Surgery, University Heart Center Hamburg.

出版信息

J Vis Exp. 2014 May 14(87):51459. doi: 10.3791/51459.

DOI:10.3791/51459
PMID:24893977
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4186352/
Abstract

Various in vivo laboratory rodent models for the induction of artery stenosis have been established to mimic diseases that include arterial plaque formation and stenosis, as observed for example in ischemic heart disease. Two highly reproducible mouse models - both resulting in artery stenosis but each underlying a different pathway of development - are introduced here. The models represent the two most common causes of artery stenosis; namely one mouse model for each myointimal hyperplasia, and atherosclerosis are shown. To induce myointimal hyperplasia, a balloon catheter injury of the abdominal aorta is performed. For the development of atherosclerotic plaque, the ApoE -/- mouse model in combination with western fatty diet is used. Different model-adapted options for the measurement and evaluation of the results are named and described in this manuscript. The introduction and comparison of these two models provides information for scientists to choose the appropriate artery stenosis model in accordance to the scientific question asked.

摘要

已经建立了各种用于诱导动脉狭窄的体内实验啮齿动物模型,以模拟包括动脉斑块形成和狭窄在内的疾病,例如在缺血性心脏病中观察到的情况。这里介绍了两种高度可重复的小鼠模型——两者都导致动脉狭窄,但各自有不同的发展途径。这些模型代表了动脉狭窄的两种最常见原因;即每种模型分别展示了肌内膜增生和动脉粥样硬化。为了诱导肌内膜增生,对腹主动脉进行球囊导管损伤。为了形成动脉粥样硬化斑块,使用ApoE -/-小鼠模型并结合西方高脂饮食。本手稿中列出并描述了针对结果测量和评估的不同模型适配选项。这两种模型的介绍和比较为科学家根据所提出的科学问题选择合适的动脉狭窄模型提供了信息。

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本文引用的文献

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Effect of 7-difluoromethyl-5, 4'-dimethoxygenistein on aorta atherosclerosis in hyperlipidemia ApoE(-/-) mice induced by a cholesterol-rich diet.7-二氟甲基-5,4'-二甲氧基大豆苷元对高脂饮食诱导的高脂血症ApoE(-/-)小鼠主动脉动脉粥样硬化的影响。
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Human internal mammary artery (IMA) transplantation and stenting: a human model to study the development of in-stent restenosis.人乳内动脉(IMA)移植与支架置入:一种用于研究支架内再狭窄发展的人体模型。
J Vis Exp. 2012 May 9(63):e3663. doi: 10.3791/3663.
4
Ultrasound guidance for the creation of a small animal model of aortic injury.超声引导下建立小型动物主动脉损伤模型。
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Npp1 promotes atherosclerosis in ApoE knockout mice.Npp1 促进载脂蛋白 E 基因敲除小鼠的动脉粥样硬化。
J Cell Mol Med. 2011 Nov;15(11):2273-83. doi: 10.1111/j.1582-4934.2011.01327.x.
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Pathogenesis of neointima formation following vascular injury.血管损伤后新生内膜形成的发病机制。
Cardiovasc Hematol Disord Drug Targets. 2011 Mar 1;11(1):30-9. doi: 10.2174/187152911795945169.
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