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首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >Effects of the chemokine CCL2 on blood-brain barrier permeability during ischemia-reperfusion injury.
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Effects of the chemokine CCL2 on blood-brain barrier permeability during ischemia-reperfusion injury.

机译：趋化因子CCL2对缺血再灌注损伤时血脑屏障通透性的影响。

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摘要

The chemokine CCL2 is considered as one of the main effectors driving postischemic infiltration of monocytes into the brain parenchyma. New experimental data, however, suggest that CCL2 could also participate in blood-brain barrier (BBB) 'opening' during the transmigration of monocytes. The current study examines the role of CCL2 in regulating BBB permeability after ischemia in vitro. To address this issue, an in vitro BBB model (coculture of astrocytes and brain endothelial cells) was subjected to 5 h of oxygen glucose deprivation, followed by reoxgenation (in vitro ischemia/reperfusion (I/R)) for 0 to 48 h. During reperfusion, there was a biphasic enhancement of barrier permeability, with a 200-fold increase in barrier permeability to FITC-albumin at 6 h and a further period of disruption around 24 h. The latter coincided with increased secretion of CCL2 by both astrocytes and brain endothelial cells and increased levels of the CCL2 receptor, CCR2. Applying antisense oligonucleotide or neutralizing antibody to block CCL2 significantly decreased I/R-induced enhancement of BBB permeability (approximately twofold) and redistribution of tight-junction (TJ) proteins (occludin, zonula occluden-1, 2, claudin-5). Similarly, absence of CCR2 from endothelial cells caused stabilization of TJ complexes and decreased the permeability of brain endothelial barrier during in vitro I/R. These data suggest CCL2/CCR2 has an important role in regulating brain endothelial permeability and might be a potential novel therapeutic target for stroke.
机译：趋化因子CCL2被认为是驱动单核细胞缺血后浸润进入脑实质的主要效应器之一。然而，新的实验数据表明，CCL2也可能在单核细胞的迁移过程中参与血脑屏障（BBB）的“开放”。目前的研究探讨了CCL2在体外缺血后调节BBB通透性中的作用。为了解决这个问题，对体外BBB模型（星形胶质细胞和脑内皮细胞的共培养）进行5 h氧葡萄糖剥夺，然后再进行氧合（体外缺血/再灌注（I / R））0至48 h。在再灌注过程中，屏障通透性双相增强，在6小时时对FITC-白蛋白的屏障通透性增加了200倍，在大约24小时后又发生了进一步的破坏。后者与星形胶质细胞和脑内皮细胞分泌CCL2的增加以及CCL2受体CCR2的水平增加相吻合。应用反义寡核苷酸或中和抗体来阻断CCL2，可显着降低I / R诱导的BBB通透性增强（大约两倍）并减少紧密连接（TJ）蛋白（occludin，zonula occluden-1、2，claudin-5）的重新分布。同样，在体外I / R期间，内皮细胞中CCC2的缺失会导致TJ复合物的稳定并降低脑内皮屏障的通透性。这些数据表明，CCL2 / CCR2在调节脑内皮渗透性中具有重要作用，并且可能是中风的潜在新治疗靶标。

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