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二次修改S100B影响抗粉样β聚合活性和阿尔茨海默病病理学

Romina Coelho^1,2, Chiara A De Benedictis^3,4, Ann Katrin Sauer^3,4,5

¹BioISI-Instituto de Biosistemas e Ciências Integrativas, Faculdade de Ciências, Universidade de Lisboa, 1749-016 Lisboa, Portugal.

International journal of molecular sciences

|February 10, 2024

概括

氧化S100B蛋白在阿尔茨海默氏病模型中显示出对粉样β聚合和毒性增强的保护作用. 这表明了一种新的治疗策略,涉及修改后的S100B用于神经保护.

科学领域:

神经科学是一个神经科学.
生物化学生物化学
分子生物学分子生物学

背景情况:

蛋白质聚合物,如粉样β (Aβ),是阿尔茨海默病 (AD) 的标志.
作为一种促炎性细胞因子的S100B,对Aβ聚合和毒性表现出非常规的保护作用.
在AD中的氧化环境可能会影响S100B的功能.

研究的目的:

研究细胞外氧化条件如何影响S100B对Aβ的保护活动.
确定S100B氧化是否增强其抑制Aβ聚合和毒性的能力.

主要方法:

轻微氧化S100B蛋白质. 这是一种轻微的氧化.
质谱测量用于识别氧化残留物 (甲氨酸).
结构分析 (折叠,稳定性,四元结构).
在Aβ聚合动力学测试中.
细胞培养模型评估Aβ毒性救援和下游细胞因子调节 (IL-17,IFN-α2).

主要成果:

在S100B中证实了甲氨酸残留的氧化,但没有影响其结构或稳定性.
与原生S100B相比,氧化S100B显示了Aβ聚合的增强抑制.
氧化S100B在细胞培养中从Aβ诱导的毒性中提供了更大的救援.
S100B氧化破坏了正反循环,改变了IL-17和IFN-α2的表达.

结论:

细胞外氧化增强了S100B对Aβ聚合和毒性的保护性伴侣活性.
氧化S100B为阿尔茨海默病提供了一个有前途的治疗点.
S100B氧化影响下游炎症通路,与AD病变发生相关.

关键词:

这是阿尔茨海默氏症.在S100蛋白质中.氨基βββββββββββββββββββββββββ 细胞因子细胞因子分子的陪伴者是分子的陪伴者.神经退行症的神经退行症神经炎症是一种神经炎症.氧化过程中的氧化.

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