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TFEB/LAMP2有助于PM_0.2诱导的自酶体功能障碍和星球细胞中的α-synuclein失调

Ben Li¹, Ting Liu¹, Yongmei Shen²

¹School of Public Health, Shanxi Medical University, Taiyuan 030000, China.

Journal of environmental sciences (China)

|June 6, 2024

概括

大气中的微粒 (PM0.2) 促进星体细胞中的α-synuclein病理,增加阿尔茨海默氏症和帕金森病的风险. 针对TFEB/LAMP2可以抵消这种PM0.2毒性.

科学领域:

神经科学是一个神经科学.
环境健康环境健康
细胞生物学细胞生物学

背景情况:

大气中的颗粒物 (PM) 与阿尔茨海默氏症和帕金森症等神经退行性疾病的风险增加有关.
天体细胞的作用和PM诱导α-synuclein (α-syn) 病理的特定机制仍然不清楚.
众所周知,暴露于PM会加剧α-syn病理,这是帕金森病的标志.

研究的目的:

调查颗粒大小<200 nm (PM0.2) 的颗粒暴露如何在小鼠和初级星球细胞中诱导α-syn病理.
在实验室中评估拉巴胺素抑制剂 (PP242) 的哺乳动物标对PM0.2诱导的α-syn病理学的影响.
阐明PM0.2相关神经退行症中涉及星体和自的分子机制.

主要方法:

对ICR小鼠和初级星球细胞暴露于PM0.2.2.
对暴露受试者的α-syn病理,质细胞激活和自标志物 (LC3II,LAMP2,CTSB,Cathepsin D) 的分析.
在体外评估星球细胞中的炎症反应和α-syn降解.
研究转录因子EB (TFEB) 局部化和PP242治疗的影响.

主要成果:

在小鼠中,暴露于PM0.2诱导了α-syn病理,质激活和抑制了自.
在体外,PM0.2触发了炎症反应,并通过受损的 lysosomal-associated membrane protein 2 (LAMP2) 介导的自细胞中破坏了α-syn降解.
PP242治疗通过增强TFEB核局部化和增加关键的自-溶酶体蛋白 (LC3II,LAMP2,CTSB,Cathepsin D) 来恢复α-syn降解.

结论:

暴露于PM0.2会促进星体细胞中的α-syn病理性失调.
这项研究提供了有关PM0.2如何增加帕金森病风险的机制性见解.
TFEB和LAMP2代表了减轻神经退行性疾病中PM0.2毒性的有前途的治疗标.

关键词:

星球细胞是星球细胞.自 - 溶酶体自 - 溶酶体自 PM{0.2}) 的情况.α-Synuclein 是一种蛋白质.

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