血管内皮钙黏蛋白和 p120 连环蛋白在动物实验性颅内动脉瘤形成中的作用。
Role of Vascular Endothelial-Cadherin and p120-Catenin in the Formation of Experimental Intracranial Aneurysm in Animals.
机构信息
Department of Neurosurgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, P.R. China; Department of Neurosurgery, Renji Hospital, School of Medicine of Shanghai Jiao Tong University, Shanghai, P.R. China.
Department of Neurosurgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, P.R. China; Department of Neurosurgery, Fudan University Huashan Hospital, Shanghai, P.R. China.
出版信息
World Neurosurg. 2019 Aug;128:e177-e184. doi: 10.1016/j.wneu.2019.04.077. Epub 2019 Apr 14.
BACKGROUND
Dysfunction of endothelial cells (ECs) constitutes a critical factor in the formation of intracranial aneurysms (IAs). However, little is known about the response of ECs to hemodynamic insults and its contribution to IA formation.
METHODS
IAs models were constructed in both adult female New Zealand white rabbits and male Sprague-Dawley rats. Morphologic changes of vessel wall were detected by hematoxylin and eosin staining. Molecular and cellular changes, including p120-catenin (p120ctn) and vascular endothelial-cadherin, in the median sagittal section of the artery bifurcation were analyzed by fluorescent staining.
RESULTS
Destructive aneurysmal remodeling and the formation of morphologic IAs were observed at the basilar termini of experimental rabbits and the anterior cerebral artery-olfactory artery bifurcation of rats. The expression of p120ctn colocalized with vascular endothelial-cadherin in ECs decreased. Moreover, the expression of p120ctn colocalized with nucleus of ECs increased. These events suggested that p120ctn was transported from the membrane to the nucleus of ECs.
CONCLUSIONS
The potential mechanism, that IAs are always localizing in the bifurcation apices, may be that the endothelium injury of vessel wall can be induced by different hemodynamic conditions. Hemodynamic changes in artery bifurcation may initiate the formation of IAs.
背景
内皮细胞（ECs）功能障碍是颅内动脉瘤（IAs）形成的一个关键因素。然而，对于 ECs 对血流动力学损伤的反应及其对 IA 形成的贡献知之甚少。
方法
在成年雌性新西兰白兔和雄性 Sprague-Dawley 大鼠中构建了 IA 模型。通过苏木精和伊红染色检测血管壁的形态变化。通过荧光染色分析动脉分叉中 p120-catenin（p120ctn）和血管内皮钙黏蛋白等分子和细胞变化。
结果
在实验兔的基底末端和大鼠的大脑前动脉-嗅动脉分叉处观察到破坏性的动脉瘤重塑和形态学 IA 的形成。p120ctn 与血管内皮钙黏蛋白在 ECs 中的共表达减少。此外，p120ctn 与 ECs 核的共表达增加。这些事件表明 p120ctn 从膜转运到 ECs 的核内。
结论
IA 总是定位于分叉顶点的潜在机制可能是血管壁内皮损伤可由不同的血流动力学条件引起。动脉分叉处的血流动力学变化可能引发 IA 的形成。
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