内毒素脂多糖致血脑屏障紧密连接改变的分子机制研究
基本信息
结项摘要
本项目利用体外血脑屏障(BBB)模型，结合小干扰RNA、质粒构建、免疫沉淀、免疫印迹和激光扫描共聚焦等研究策略，探讨感染性脑损伤时，LPS致BBB紧密连接(BBB-TJ)改变的分子机制和信号调控。我们开创性地将p115RhoGEF与RhoA、NF-κB结合一起进行研究，提示LPS在激活NF-κB、RhoA同时，RhoA又通过酪氨酸激酶再促进NF-κB进一步活化，然后两者共同参与对BBB-TJ调控。在此我们首次提出LPS介导的TNF-α经p115RhoGEF途径促进RhoA活化在BBB-TJ变化中的重要调控作用，同时将证实RhoA和TNF-α通过Rho 激酶，使BBB紧密连接蛋白磷酸化，Actin重组，Occludin -ZO-Actin连接、分布和表达异常，最终使BBB通透性增加。对这一问题的深入研究，将从全新角度首次阐明感染性脑损伤时BBB-TJ改变的分子机制及调控，为其治疗提供新思路。
项目摘要
项目成果
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数据更新时间：2023-05-31
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