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在诱导的细胞损伤中,N⁶-甲基亚诺辛修饰和未折叠蛋白质反应的变化

Nan Wang¹, Jiao Dai², Rongxian Li¹

¹School of Public Health, Dali University, Dali, Yunnan, PR China; Institute of Preventive Medicine, Dali University, Dali, Yunnan, PR China.

Ecotoxicology and environmental safety

|October 18, 2025

概括

暴露会增加细胞亡和氧化应激. RNA m⁶A 修饰和展开的蛋白质响应 (UPR) 信号与这种诱导的损伤有关,这表明潜在的治疗标.

科学领域:

腎臟毒理學腎臟毒理學
对于RNA的表观遗传学
细胞应激反应的细胞应激反应

背景情况:

在诱导的损伤中,RNA N6 - - 甲基氨酸 (m6A) 修饰和未折叠蛋白反应 (UPR) 信号的作用仍然不清楚.
是一种具有毒性的金属,已知会诱导细胞损伤.
了解这些分子机制对于解决毒性的问题至关重要.

研究的目的:

调查m6A修饰和UPR信号在诱导的细胞损伤中的参与.
探索m⁶A调节蛋白,UPR信号分子和损伤之间的关系.
确定潜在的分子标,以减轻的毒性.

主要方法:

用硫酸 (CdSO) 治疗小鼠以诱导损伤.
评估亡速率和脏组织中的氧化应激.
对m6A修饰水平和关键m6A调控蛋白的表达 (Mettl3,Mettl16,Alkbh5,Fto,Ythdc2,Ythdf2) 的分析.
评估UPR信号分子 (Atf4,Atf6,Perk,Xbp1,Grp78,Bax,Caspase-12,Bcl-2) 的蛋白质表达.
在m⁶A级和UPR信号之间进行相关性分析.
免疫光研究以确定Ythdf2和Xbp1.1的局部化.

主要成果:

治疗显著增加了细胞亡和氧化应激.
综合RNAm6A修饰水平和m6A调节蛋白的表达随着度的增加而升高.
在接受治疗的小鼠中,UPR信号分子的调节上升,而抗亡蛋白Bcl-2的调节下降.
在m⁶A修饰水平和UPR信号分子表达之间观察到显著的相关性.
Ythdf2从细胞质转移到细胞核,Xbp1水平在脏中增加,尽管它们的分布不同.

结论:

两种m6A修饰和UPR信号分子都在诱导的组织损伤中发挥着关键作用.
一个由特定蛋白质调节的修饰似乎在毒性的背景下调节了UPR信号通路.
这些发现为确定毒性治疗标提供了一个框架,将RNA表观遗传与UPR信号联系起来.

关键词:

是的组成部分.脱甲基酶的使用方法甲基结合蛋白是一种甲基结合蛋白.甲基转移酶的使用方法 N(6) - - 甲基氨酸.不折叠的蛋白质反应反应

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