在缺血性中风后,METTL14通过KAT3B-STING轴调节微质/巨细胞两极分化和NLRP3炎症酶激活

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¹Department of Rehabilitation Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu 610072, Sichuan, China.

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|August 4, 2023

概括

甲基转移酶样14 (METTL14) 促进缺血性中风脑损伤,通过上调M1微质极化和NLRP3炎症组/炎症灭亡轴. 通过抑制这些通路,METTL14的枯竭减轻了损伤.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

N6-甲基氨酸 (m6A) 在缺血性中风中至关重要.
甲基转移酶样14 (METTL14) 在缺血性中风中的特定作用目前尚不清楚.

研究的目的:

研究METTL14在缺血性中风中的作用.
阐明METTL14在脑损伤中的潜在分子机制.

主要方法:

在体内中脑动脉封闭 (MCAO) 的老鼠模型.
在HAPI细胞中的体外氧-葡萄糖剥夺/再输液 (OGD/R).
对METTL14,KAT3B,STING和H3K27ac表达和修饰的分析.

主要成果:

在MCAO和OGD/R后的微质/巨细胞中,METTL14表达被上调.
通过m6A修改KAT3BmRNA,METTL14增强了KAT3B的表达.
KAT3B通过增强H3K27ac在STING促进器上增加了STING表达.
通过KAT3B-STING通路,METTL14促进了M1两极化和NLRP3炎症组/热轴.
在MCAO大鼠中,METTL14枯竭减少了脑损伤,因为它抑制了M1-样的微质/巨细胞两极分化和NLRP3炎症组/炎症灭亡轴.

结论:

减少METTL14可以缓解MCAO诱导的大脑损伤.
METTL14可能会将微质/巨细胞两极分化从M1转移到M2.
由于METTL14的减少,抑制了微质/巨细胞中的NLRP3炎症酶/炎症酶轴.

关键词:

缺血性中风是因为缺血性中风.在METTL14中,使用的是METTL14 微质的极化是微质的极化在NLRP3炎症酶体中,NLRP3炎症

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