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Poldip2 mediates blood-brain barrier disruption and cerebral edema by inducing AQP4 polarity loss in mouse bacterial meningitis model.
CNS Neuroscience & Therapeutics ( IF 5.5 ) Pub Date : 2020-08-12 , DOI: 10.1111/cns.13446
Meng Gao 1 , Weitian Lu 1, 2 , Yue Shu 1 , Zhengyu Yang 1 , Shanquan Sun 1, 2 , Jin Xu 1, 2 , Shengwei Gan 1, 2 , Shujuan Zhu 1, 2 , Guoping Qiu 1, 2 , Fei Zhuo 1, 2 , Shiye Xu 1, 2 , Yiying Wang 1 , Junhong Chen 1 , Xuan Wu 3 , Juan Huang 1, 2
Affiliation  

Specific highly polarized aquaporin‐4 (AQP4) expression is reported to play a crucial role in blood‐brain barrier (BBB) integrity and brain water transport balance. The upregulation of polymerase δ‐interacting protein 2 (Poldip2) was involved in aggravating BBB disruption following ischemic stroke. This study aimed to investigate whether Poldip2‐mediated BBB disruption and cerebral edema formation in mouse bacterial meningitis (BM) model occur via induction of AQP4 polarity loss.

中文翻译:

Poldip2 通过在小鼠细菌性脑膜炎模型中诱导 AQP4 极性丧失来介导血脑屏障破坏和脑水肿。

据报道,特定的高度极化水通道蛋白 4 (AQP4) 表达在血脑屏障 (BBB) 完整性和脑水运输平衡中起着至关重要的作用。聚合酶 δ 相互作用蛋白 2(Poldip2)的上调参与了缺血性卒中后 BBB 破坏的加重。本研究旨在探讨小鼠细菌性脑膜炎 (BM) 模型中 Poldip2 介导的 BBB 破坏和脑水肿形成是否通过诱导 AQP4 极性丧失而发生。
更新日期:2020-08-12
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