Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Department of Pathophysiology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, China.
FASEB J. 2018 Jun;32(6):3133-3148. doi: 10.1096/fj.201701121R. Epub 2018 Jan 18.
Blood-brain barrier (BBB) disruption caused by reperfusion injury after ischemic stroke is an intractable event conducive to further injury. Brain pericytes play a vital role in maintaining BBB integrity by interacting with other components of the BBB. In this study, we found that sphingosine-1-phosphate receptor (S1PR)2 expressed in pericytes was significantly up-regulated after ischemia in vivo and in vitro. By using a S1PR2 antagonist (JTE-013), we showed that S1PR2 plays a critical role in the induction of BBB permeability of transient middle cerebral artery occlusion (tMCAO) rats and the in vitro BBB model. Furthermore, we discovered that S1PR2 may decrease N-cadherin expression and increase pericyte migration via NF-κB p65 signal and found that S1PR2 could be regulated by miR-149-5p negatively, which was decreased in the ischemic boundary zone and cultured pericytes after ischemia. Overexpression of miR-149-5p in cultured pericytes substantially increased N-cadherin expression and decreased pericyte migration, which decreased BBB leakage in the in vitro model. Up-regulating miR-149-5p by intracerebroventricular injection of agomir-149-5p attenuated BBB permeability and improved the outcomes of tMCAO rats significantly. Thus, our data suggest that miR-149-5p may serve as a potential target for treatment of BBB disruption after ischemic stroke.-Wan, Y., Jin, H.-J., Zhu, Y.-Y., Fang, Z., Mao, L., He, Q., Xia, Y.-P., Li, M., Li, Y., Chen, X., Hu, B. MicroRNA-149-5p regulates blood-brain barrier permeability after transient middle cerebral artery occlusion in rats by targeting S1PR2 of pericytes.
血脑屏障(BBB)在缺血性中风后的再灌注损伤中被破坏,这是一个有利于进一步损伤的棘手事件。脑周细胞通过与 BBB 的其他成分相互作用,在维持 BBB 完整性方面发挥着至关重要的作用。在这项研究中,我们发现周细胞中表达的鞘氨醇-1-磷酸受体(S1PR)2在体内和体外缺血后显著上调。通过使用 S1PR2 拮抗剂(JTE-013),我们表明 S1PR2 在短暂性大脑中动脉闭塞(tMCAO)大鼠和体外 BBB 模型中 BBB 通透性的诱导中起着关键作用。此外,我们发现 S1PR2 可能通过 NF-κB p65 信号降低 N-钙粘蛋白的表达并增加周细胞的迁移,并且发现 S1PR2 可以被 miR-149-5p 负向调节,miR-149-5p 在缺血边界区和缺血后培养的周细胞中减少。在培养的周细胞中过表达 miR-149-5p 可显著增加 N-钙粘蛋白的表达并减少周细胞的迁移,从而减少体外模型中的 BBB 渗漏。通过侧脑室注射 agomir-149-5p 上调 miR-149-5p 可显著减轻 tMCAO 大鼠的 BBB 通透性并改善其预后。因此,我们的数据表明,miR-149-5p 可能成为治疗缺血性中风后 BBB 破坏的潜在靶点。-万玉,金慧静,朱艳艳,方臻,毛蕾,何琴,夏宇鹏,李萌,李艳,陈鑫,胡兵。miR-149-5p 通过靶向周细胞的 S1PR2 调节大鼠短暂性大脑中动脉闭塞后血脑屏障通透性。