A simple method of plaque rupture induction in apolipoprotein E-deficient mice
A simple method of plaque rupture induction in apolipoprotein E-deficient mice
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DOI：
10.1161/01.atv.0000219687.71607.f7
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发表时间：
2006-06-01
影响因子：
8.7
通讯作者：
Iguchi, Akihisa
中科院分区：
文献类型：
--
作者：
Sasaki, Takeshi;Kuzuya, Masafumi;Iguchi, Akihisa
Objective -动脉粥样硬化斑块破裂的小鼠模型的发展。方法和结果-雄性载脂蛋白E（apoE）缺陷小鼠（9周龄）的左颈总动脉在其分叉近端结扎。在标准饮食4周后，小鼠接受聚乙烯袖套放置在结扎部位近端，然后在特定时间点处理动物进行形态学研究。在apoE缺陷小鼠中结扎颈动脉4周可诱导显著的内膜增生，这是一种富含脂质和胶原的病变，含有大量巨噬细胞、T淋巴细胞和平滑肌细胞。随后，袖口放置诱发斑块内出血和斑块破裂，纤维蛋白（原）阳性管腔血栓在这一地区伴随着胶原蛋白含量的减少，以及增加在内膜中的凋亡细胞在几天后cuff placement.Conclusions -我们证明了人类斑块破裂，这是简单，快速，高效的小鼠模型。该模型不仅有助于我们了解人类斑块破裂的机制，而且有助于我们评估未来各种已知和未知的药物。
Objective - The development of a murine model of atherosclerotic plaque rupture.Methods and Results - The left common carotid arteries of male apolipoprotein E ( apoE)-deficient mice ( 9 weeks old) were ligated just proximal to their bifurcations. After 4 weeks on a standard diet, the mice received polyethylene cuff placement just proximal to the ligated site, and the animals were then processed for morphological studies at specific time points. Ligation of the carotid artery in apoE-deficient mice for 4 weeks induced marked intimal hyperplasia, which is a lipid- and collagen-rich lesion that contains a number of macrophages, T lymphocytes, and smooth muscle cells. Subsequently, the cuff placement evoked intraplaque hemorrhage and plaque rupture with fibrin( ogen)-positive luminal thrombus in this region accompanying a decrease in collagen content as well as an increase in apoptotic cells in the intima within a few days after cuff placement.Conclusions - We demonstrated the murine model of human plaque rupture, which is simple, fast, and highly efficient. This model would help us not only to understand the mechanism of human plaque rupture but also to assess various already-known and as-yet-unknown agents in the future.