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TFEB通过激活GAL3/TRIM16轴依赖的溶解细胞和缓解溶解体功能障碍来改善DEHP诱导的神经毒性

Hengrui Xing^1,2,3,4, Panpan Xu^1,2,3,4, Yue Ma^1,2,3,4

¹Department of Preventive Medicine, School of Medicine, Shihezi University, Shihezi, People's Republic of China.

Environmental toxicology

|March 15, 2024

概括

二甲基甲酸 (DEHP) 通过破坏溶解体和抑制溶解体,一种由转录因子EB (TFEB) 调节的过程,引起神经毒性. 恢复TFEB功能可能会防止DEHP诱导的神经细胞死亡.

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
毒理学毒理学毒理学

背景情况:

-2-乙烯基) 甲酸盐 (DEHP) 是一种广泛使用的可塑剂,已被证明具有神经毒性作用.
在DEHP诱导的神经毒性背后的精确机制,特别是关于细胞降解途径,尚未完全理解.

研究的目的:

研究 lysosomal 功能和 lysophagy 在 DEHP 诱导的神经毒性的作用.
阐明转录因子EB (TFEB) 在这些过程中的调节功能.

主要方法:

使用的体外模型:暴露于DEHP的SH-SY5Y和HT22神经元细胞.
评估了溶酶体损伤,自性降解标志物 (LC3II,p62) 和关键蛋白质的表达 (TFEB,GAL3,TRIM16,PARP).
研究了TFEB过度表达对DEHP诱导的细胞反应的影响.

主要成果:

暴露于DEHP诱导了溶酶体损伤,功能障碍和自细胞降解的受损.
DEHP降低了TFEB,GAL3和TRIM16的调节,抑制了依赖GAL3/TRIM16的溶解酶并促进了细胞亡.
过度表达TFEB挽救了溶酶体功能,激活了溶酶体,并减少了DEHP诱导的神经元亡.

结论:

DEHP的神经毒性涉及溶解体功能障碍和通过TFEB/GAL3/TRIM16通路抑制溶解体.
损坏的溶酶体的清除受损有助于神经元亡.
TFEB在调节溶解细胞的过程中起着至关重要的作用,是DEHP神经毒性的潜在治疗点.

关键词:

在DEHP中,DEHP是DEHP.在GAL3/TRIM16轴上美国联邦税务法 (TFEB)lysophagy lysophagy 是一种消化性消化方式.lysosomal 功能溶解体功能溶解体功能

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Lysosomal Hydrolases

Lysosomal Hydrolases

Lysosomes are the site for the degradation of macromolecules and biological polymers released during membrane trafficking events such as secretory, endocytic, autophagic, and phagocytic pathways. The membrane-enclosed area of the lysosome, called the lumen, contains hydrolytic enzymes active in an acidic environment. These acid hydrolases are functional at a pH between 4.5 and 5 and are involved in cellular processes such as cell signaling, energy metabolism, restoration of the plasma membrane,...