Tracing the endocytosis of claudin-5 in brain endothelial cells.
Tracing the endocytosis of claudin-5 in brain endothelial cells.
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DOI：
10.1007/978-1-61779-185-7_22
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发表时间：
2011
影响因子：
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通讯作者：
S. Stamatovic;R. Keep;A. Andjelkovic
中科院分区：
文献类型：
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作者：
S. Stamatovic;R. Keep;A. Andjelkovic
Claudin-5是一种跨膜紧密连接蛋白，在脑内皮细胞（血脑屏障的部位）中高度表达。脑内皮紧密连接复合物的性质被认为依赖于claudin-5细胞-细胞相互作用，使该蛋白在维持脑内皮屏障完整性中发挥主要作用。因此，claudin-5功能的改变可导致细胞旁途径的“开放”和脑内皮屏障通透性的增加。作者实验室最近的工作已经确定，密蛋白-5的小窝依赖性内化/再循环是在促炎介质存在的情况下脑内皮细胞旁渗透性短暂增加的潜在机制。这里提出的生物化学和显微镜技术被用来调查在细胞旁通透性的变化过程中的密蛋白-5的贩运。
Claudin-5 is a transmembrane tight junction protein highly expressed in brain endothelial cells, the site of the blood–brain barrier. The properties of the brain endothelial tight junction complex are considered to be dependent on claudin-5 cell–cell interaction, putting this protein in a position to play a major role in the maintenance of brain endothelial barrier integrity. Thus, alterations in claudin-5 function can lead to “opening” of the paracellular route and increased brain endothelial barrier permeability. Recent work from the authors’s laboratory has established that caveolae-dependent internalization/recycling of claudin-5 is a mechanism underlying transient increases in brain endothelial paracellular permeability in the presence of pro-inflammatory mediators. The biochemical and microscopic techniques presented here were used to investigate trafficking of claudin-5 during those changes in paracellular permeability.