The temporal expression patterns of fibronectin and its receptors-α5β1 and αvβ3 integrins on blood vessels after cerebral ischemia
The temporal expression patterns of fibronectin and its receptors-α5β1 and αvβ3 integrins on blood vessels after cerebral ischemia
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DOI：
10.3233/rnn-140491
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发表时间：
2015-01-01
影响因子：
2.8
通讯作者：
Li, Longxuan
中科院分区：
文献类型：
--
作者：
Huang, Qijuan;Chen, Bing;Li, Longxuan
目的：我们先前证明，缺血后7天，缺血半暗带中的血管生成血管显示纤连蛋白（Fn）及其受体α 5 β 1和α v β 3整合素的强烈上调。目前的研究的目的是精确地定义的时间过程中的血管生成反应和胶质细胞激活后，实验性ischemia.Methods：雄性C57 B1/6小鼠缺血90分钟，大脑中动脉暂时闭塞，然后再灌注。血管重塑和胶质细胞活化，然后检查这些小鼠的大脑后0，1，2，4，7和14天postischemia.Results：免疫荧光研究表明，在缺血半暗带，血管密度增加到第14天。相反，在缺血核心内，血管密度下降，在第4天达到低点，但随后开始增加。在半影区，Fn和α 5和β 3整合素的表达在第7天达到峰值，这正好与最大的内皮proliferation.Conclusions：我们的研究结果表明，上调Fn-α 5 β 1和α v β 3整合素轴血管刺激BEC增殖在早期阶段的血管生成缺血后。这可能形成新的治疗策略的基础，旨在促进脑缺血后的血管生成。
Purpose: We previously demonstrated that 7 days post-ischemia, angiogenic vessels in the ischemic penumbra show strong upregulation of fibronectin (Fn) and its receptors, alpha 5 beta 1 and alpha v beta 3 integrins. The aim of the current study was to precisely define the time-course of angiogenic responses and glial activation following experimental ischemia in the mouse.Methods: Male C57Bl/6 mice were subject to 90 minutes of ischemia by temporary occlusion of the middle cerebral artery followed by reperfusion. Vascular remodeling and glial activation were then examined in the brains of these mice after 0, 1, 2, 4, 7 and 14 days post-ischemia.Results: Immunofluorescent studies demonstrated that in the ischemic penumbra, blood vessel density increased up to day 14. In contrast, within the ischemic core, vessel density declined, reaching a low point at day 4, but then started to increase. In the penumbra, expression of Fn and the alpha 5 and beta 3 integrins peaked at day 7, and this coincided exactly with maximal endothelial proliferation.Conclusions: Our results suggest that upregulation of the Fn-alpha 5 beta 1 and alpha v beta 3 integrin axis on blood vessels stimulates BEC proliferation at an early stage of angiogenesis post-ischemia. This could form the basis of novel therapeutic strategies aimed at promoting angiogenesis following cerebral ischemia.