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在人类ALS模型中,TNFα阻止了FGF4介导的星细胞功能障碍和反应性的救援

Erika Velasquez¹, Ekaterina Savchenko¹, Sara Marmolejo-Martínez-Artesero²

¹iPSC Laboratory for CNS Disease Modelling, Department of Experimental Medical Science, BMC D10, Lund University, 22184 Lund, Sweden; Strategic Research Area MultiPark, Lund University, Lund SE-221 84, Sweden; Lund Stem Cell Center, Lund University, Lund SE-221 84, Sweden.

Neurobiology of disease

|October 3, 2024

概括

肌缩侧面硬化症 (ALS) 星球细胞是功能失调和反应性的. 纤维细胞生长因子4 (FGF4) 在体外和体内逆转了一些天体细胞问题,但神经炎症阻碍了运动神经元的保护.

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
遗传学是一个遗传学.

背景情况:

星球细胞在肌缩性侧面硬化症 (ALS) 中至关重要,但它们的神经毒性表型尚不清楚.
在ALS中,运动神经元退化与天体细胞功能障碍有关.
研究ALS天体细胞的早期细胞变化对于了解疾病进展至关重要.

研究的目的:

为了研究早期细胞通路和网络变化的人类星细胞与ALS相关的突变.
识别ALS天体细胞中改变的蛋白质及其与先天免疫路径的联系.
评估纤维细胞生长因子 (FGFs) 在逆转ALS天体细胞表型方面的治疗潜力.

主要方法:

从具有SOD1 A4V突变的诱导多能干细胞 (iPSC) 中生成的人类星球细胞.
进行蛋白质组分析来比较ALS和控制星球细胞.
在实验室中将FGFs给ALS天体细胞和FGF4给SOD1 G93A小鼠模型.

主要成果:

ALS天体细胞表现出功能障碍和反应性,在cGAS-STING通路中的蛋白质发生变化.
在实验室中,FGF4逆转了ALS天体细胞功能障碍和反应性.
在体内,FGF4降低了星球细胞的反应性,但没有阻止运动神经元的死亡,可能是由于TNFα介导的炎症.

结论:

患有ALS相关突变的人类星细胞本质上是功能障碍和免疫反应.
准星细胞功能障碍和反应性是ALS治疗的潜在策略.
神经炎症使FGF4在保护运动神经元中的有效性变得复杂.

关键词:

肌缩性侧面硬化症 (AMLS) 是一种疾病.星球细胞是星球细胞.纤维细胞生长因子的成长因子诱导的多能干细胞干细胞天生的免疫系统天生的免疫系统.蛋白质组学是指蛋白质组学.瘤亡因子-阿尔法

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