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Updated: Jul 26, 2025

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由Ogt介导的O-GlcNAcylation通过调节NF-κB信号通路来抑制星体细胞的激活

Xiaoxue Dong^1,2, Liqi Shu³, Jinyu Zhang^1,2

¹The Children's Hospital, National Clinical Research Center for Child Health, School of Medicine, Zhejiang University, Hangzhou, 310052, China.

Journal of neuroinflammation

|June 22, 2023

概括

缺少O-GlcNAc转移酶 (Ogt) 会激活星球细胞并损害认知功能. 用GlcNAc恢复O-GlcNAcylation可以通过调节NF-κB通路来改善认知和减少炎症.

科学领域:

神经科学是一个神经科学.
细胞生物学细胞生物学
生物化学生化学

背景情况:

O-GlcNAcylation是一种翻译后的修饰,对神经元的发育和功能至关重要.
在星球细胞中O-GlcNAc转移酶 (Ogt) 和O-GlcNAcylation的作用在很大程度上尚未被探索.

研究的目的:

为了研究Ogt介导的O-GlcNAcylation在星球细胞中的功能.
阐明Ogt在天体细胞激活和认知功能中的作用背后的分子机制.

主要方法:

使用了体内和体外模型,包括Ogt缺乏的小鼠和人类诱导的多能干细胞衍生天体细胞.
研究了Ogt和NF-κB p65之间的相互作用,以及Gsk3β的作用.
评估认知功能,星球细胞激活,炎症标志物和粉样β (Aβ) 斑块负载.

主要成果:

在小鼠中,Ogt 缺乏导致天体细胞激活,炎症和认知功能受损.
GlcNAc补充恢复了O-GlcNAcylation,抑制了天体细胞激活和炎症,并改善了认知缺陷.
奥格特与NF-κB p65相互作用,其缺乏通过Gsk3β激活NF-κB通路.
在阿尔茨海默氏病模型中,Ogt 枯竭激活了人类的天体细胞,并减少了Aβ斑块.

结论:

由Ogt介导的O-GlcNAcylation在调节星细胞激活和神经炎症方面发挥着至关重要的作用.
准星球细胞中的O-GlcNAcylation可能为认知障碍和神经退行性疾病 (如阿尔茨海默氏症) 提供治疗潜力.

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