Cerebral ischemia enhances tyrosine phosphorylation of occludin in brain capillaries
Cerebral ischemia enhances tyrosine phosphorylation of occludin in brain capillaries
复制标题
DOI：
10.1016/j.bbrc.2005.11.133
复制
发表时间：
2006-01-27
影响因子：
3.1
通讯作者：
Takeo, S
中科院分区：
文献类型：
--
作者：
Kago, T;Takagi, N;Takeo, S
脑缺血引起血脑屏障(BBB)的破坏，这种破坏可以启动脑损伤的发展。尽管血脑屏障中紧密连接复合体的分子结构已经确定，但对脑缺血后紧密连接蛋白的变化知之甚少。因此，我们研究了微球诱导脑栓塞后大鼠脑毛细血管紧密连接蛋白，即occludin和zonula occludens(ZO)-1的变化。我们证实栓塞术后闭塞素和ZO-1水平下降。栓塞组血管内皮细胞c-Src活性升高，并导致阻断素酪氨酸磷酸化水平显著升高。这些结果提示，脑缺血后血脑屏障功能障碍可能与闭合素和ZO-1水平的降低以及闭合素酪氨酸磷酸化水平的升高有关。(C)2005 Elsevier Inc.保留所有权利。
Cerebral ischemia induces disruption of the blood-brain barrier (BBB), and this disruption can initiate the development of brain injuries. Although the molecular structure of tight junctional complexes in the BBB has been identified, little is known about alterations of tight junctional proteins after cerebral ischemia. Therefore, we investigated alterations of tight junctional proteins, i.e., occludin and zonula occludens (ZO)-1, in isolated rat brain capillaries after microsphere-induced cerebral embolism. We demonstrated that the levels of occludin and ZO-1 had decreased after the embolism. The embolism also resulted in a marked increase in tyrosine phosphorylation of occludin, which was coincident with an increase in the activity of c-Src. These results suggest that a decrease in the levels of occludin and ZO-1, and an increase in tyrosine phosphorylation of occludin may play an important role in the disruption of tight junctions, which may lead to dysfunction of the BBB after cerebral ischemia. (c) 2005 Elsevier Inc. All rights reserved.