Assessments of tight junction proteins occludin, claudin 5 and scaffold proteins ZO1 and ZO2 in endothelial cells of the rat blood-brain barrier: Cellular responses to neurotoxicants malathion and lead acetate
Assessments of tight junction proteins occludin, claudin 5 and scaffold proteins ZO1 and ZO2 in endothelial cells of the rat blood-brain barrier: Cellular responses to neurotoxicants malathion and lead acetate
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DOI：
10.1016/j.neuro.2010.10.004
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发表时间：
2011-01-01
期刊：
影响因子：
3.4
通讯作者：
Ehrich, Marion
中科院分区：
文献类型：
--
作者：
Balbuena, Pergentino;Li, Wen;Ehrich, Marion
血脑屏障（BBB）是中枢神经系统（CNS）正常功能所必需的。它是由具有特殊特性的内皮细胞形成的，其赋予BBB低渗透性和高跨内皮电阻（TEER）。我们以前证明，马拉硫磷和铅，两个神经毒物广泛存在于环境中，降低TEER和增加在体外模型的血脑屏障的渗透性。在这项研究中，我们使用暴露于10（-5）M和10（-6）M醋酸铅的大鼠脑微血管内皮细胞系（RBE 4），评估了蛋白质和基因表达水平上的紧密连接破坏。马拉硫磷10（-5）M，马拉氧磷10（-6）M，及其组合。将细胞与处理一起孵育2小时、4小时、8小时、16小时和24小时。免疫印迹评估表明，治疗后紧密连接蛋白occludin和claudin 5以及支架蛋白ZO 1和ZO 2的蛋白水平降低。基因表达测定与蛋白质减少无关，表明对这些蛋白质的影响是翻译后的。(C)2010年爱思唯尔公司All rights reserved.
The blood-brain barrier (BBB) is essential for central nervous system (CNS) normal function. It is formed by endothelial cells with special characteristics, which confer the BBB with low permeability and high transendothelial electrical resistance (TEER). We previously demonstrated that malathion and lead, two neurotoxicants widely present in the environment, decrease TEER and increase permeability in in vitro models of the BBB. In this study we assessed tight junction disruption at the protein and gene expression levels using a rat brain microvascular endothelial cell line (RBE4) exposed to lead acetate at 10(-5) M and 10(-6) M. malathion at 10(-5) M, malaoxon at 10(-6) M, and their combinations. Cells were incubated with treatments for 2 h, 4 h, 8 h, 16 h, and 24 h periods. Immunoblotting assessments demonstrated that protein levels of tight junction proteins occludin and claudin 5, and scaffold proteins ZO1 and ZO2 were decreased after treatments. Gene expression determinations did not correlate with the decreases in protein, indicating that the effects on these proteins were post-translational. (C) 2010 Elsevier Inc. All rights reserved.