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破碎1-Notch1信号通路诱导M1微质破坏视网膜微血管内皮细胞的屏障功能
Xiyu Wu1,2, Haoxian Zhu1,2, Junbin Liu2
1School of Medicine, South China University of Technology, Guangzhou, China.
微质炎症有助于视网膜疾病. 这项研究揭示了M1微质中的Jagged1-Notch1通路破坏了视网膜内皮细胞屏障,影响了疾病的进展.
科学领域:
- 眼科医生 眼科 眼科
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
背景情况:
- 与微质相关的炎症是视网膜疾病发展的关键因素.
- 了解M1微质在视网膜屏障完整性中的作用对于治疗策略至关重要.
研究的目的:
- 研究M1表型微质细胞对视网膜微血管内皮细胞屏障功能的影响.
- 阐明涉及Jagged1-Notch1信号通路的潜在机制.
主要方法:
- 使用了人类微质细胞 (HMC3) 和视网膜微血管内皮细胞 (HRMEC).
- 定量PCR,西斑和ELISA评估了M1/M2标记物,细胞因子和Notch信号.
- 细胞透性,紧结蛋白和亡试验评估了屏障功能.
主要成果:
- 脂聚糖 (LPS) 在HMC3细胞中诱导M1极化,增加促炎性标记物.
- 来自M1微质的条件介质增加了HRMEC的透性,减少了紧接口蛋白 (zonula occludens-1,Occludin),并诱导了亡.
- Jagged1 抑制或 Notch1 阻塞阻止了 M1 两极分化,并保留了 HRMEC 屏障功能.
结论:
- 贾格德1-诺奇1信号通路介导M1微质诱导的视网膜内皮屏障的破坏.
- 这种机制与视网膜疾病的发病有关.
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