工程设计的Wnt7a配体在COVID-19小鼠模型中拯救了血脑屏障和认知缺陷
Troy N Trevino1, Avital B Fogel1, Guliz Otkiran1
1Department of Anatomy and Cell Biology, University of Illinois at Chicago, College of Medicine, Chicago, IL 60612, USA.
Brain : a journal of neurology
|February 2, 2024
概括
增强Wnt/β-catenin信号保护了血脑屏障,并减少了SARS-CoV-2感染后的神经炎症. 这种方法改善了认知功能和运动缺陷,为病毒引起的神经障碍提供了潜在的治疗策略.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- SARS-CoV-2 感染会导致系统性血管炎症和认知障碍.
- 连接呼吸道感染与脑血管功能障碍和神经炎症的机制尚不清楚.
- 轻微的SARS-CoV-2感染可以破坏血脑屏障 (BBB) 的完整性.
研究的目的:
- 为了确定由SARS-CoV-2失调的大脑内皮细胞中的信号通路.
- 研究Wnt/β-catenin信号传递在SARS-CoV-2引起的大脑血管功能障碍中的作用.
- 确定增强Wnt/β-catenin活性是否可以减轻感染后的神经缺陷.
主要方法:
- 在感染SARS-CoV-2 MA10的小鼠中,对大脑内皮细胞的无偏转录分析.
- 提供针对脑血管的Wnt7a配体,以增强Wnt/β-catenin活性.
- 评估BBB完整性,免疫细胞透,微质激活和认知/运动功能.
主要成果:
- SARS-CoV-2 感染抑制了大脑内皮细胞中的 Wnt/β-catenin 信号传递.
- Wnt7a配送的配合物保持了BBB完整性,并减少了神经炎症 (T细胞透,微质激活).
- 增强的Wnt/β-catenin信号改善了学习,记忆和布拉迪基尼西亚缺陷.
结论:
- 抑制Wnt/β-catenin信号传递有助于大脑血管功能障碍和SARS-CoV-2感染后的认知障碍.
- 针对性增强Wnt/β-catenin信号传递为病毒感染的神经后续提供了一个有希望的治疗途径.
- 恢复Wnt/β-catenin活性可能是改善感染后认知健康的策略.
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