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SLC38A9直接参与Tat诱导的内分泌体功能障碍和星体细胞衰老

Neda Rezagholizadeh¹, Gaurav Datta¹, Wendie A Hasler¹

¹Department of Biomedical Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND, USA.

Life science alliance

|May 5, 2025

概括

艾滋病毒-1 Tat蛋白通过破坏内酶体,在大脑中触发细胞衰老,这是由阿尔金因传感器SLC38A9.9介导的过程. 这一发现揭示了艾滋病毒相关的神经认知障碍中神经退行机制.

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
病毒学病毒学

背景情况:

细胞衰老加速衰老,并导致神经退行,包括与艾滋病毒相关的神经认知障碍.
在中枢神经系统 (CNS) 中的转录 (Tat) 蛋白质持久性与神经认知能力下降有关.
分泌的Tat通过引起内分泌体功能障碍,诱导中枢神经系统细胞中的细胞衰老.

研究的目的:

调查HIV-1 Tat是否通过人类星体细胞中依赖内解体的途径诱导细胞衰老.
为了阐明涉及TAT诱导细胞衰老的特定分子相互作用.

主要方法:

用HIV-1 Tat.治疗人类星球细胞.
对TAT内部化和与内解体蛋白相互作用的分析.
评估内分泌体功能,HIV-1 LTR交换活化和衰老标志物.

主要成果:

内化Tat与内溶酶体中的阿尔金因传感器SLC38A9相互作用.
这种相互作用导致内溶性体功能障碍.
Tat-SLC38A9的相互作用增强了HIV-1 LTR的交换活化,并诱导了星球细胞中的细胞衰老.

结论:

内分泌体功能障碍是TAT诱导的细胞衰老的关键驱动因素.
氨酸传感器SLC38A9在调解Tat对内分泌体和天体细胞衰老的影响方面发挥着至关重要的作用.
针对Tat-SLC38A9相互作用可能为艾滋病毒相关的神经认知障碍提供治疗策略.

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