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METTL14通过稳定m6A-IGF2BP3机制中的HDAC3表达来促进缺血性中风诱导的大脑损伤

Xuelin Liang¹, Songhe Yin¹, Canfang Hu¹

¹The Medical Department of Neurology, Jinshan branch of Shanghai Sixth People's Hospital, Shanghai, China.

Cell biochemistry and biophysics

|October 24, 2024

概括

甲基转移酶样14 (METTL14) 通过修改Histone Deacetylase 3 (HDAC3) 来促进缺血性中风损伤. 沉默METTL14通过通过cGAS-STING通路抑制炎症和热致死来保护大脑免受损伤.

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
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

在缺血性中风 (IS) 中,N6-甲基氨酸 (m6A) 修改至关重要.
甲基转移酶样14 (METTL14) 在IS中的作用尚不清楚.
研究大脑IS中的METTL14的功能和机制至关重要.

研究的目的:

研究METTL14在脑缺血性中风中的功能和机制.
探索METTL14在微质激活和脑损伤中的作用.
阐明IS中METTL14调节的分子通路.

主要方法:

建立了体外 (小鼠BV-2微质细胞OGD/R) 和体内 (老鼠MCAO) 缺血性中风模型.
通过qRT-PCR和西部涂抹评估了METTL14,基因组脱酶酶3 (HDAC3) 和cGAS-STING通路蛋白.
评估了细胞增殖,炎症,微质偏离,热,m6A修饰,心脏病发作量和神经学分数.

主要成果:

在缺血病和脑组织中,METTL14水平升高.
抑制METTL14抑制了微质增殖,炎症和热,并改善了脑损伤.
METTL14以依赖IGF2BP3的方式促进了HDAC3 m6A的修饰,激活了cGAS-STING通路.

结论:

METTL14通过诱导HDAC3 m6A修饰和激活cGAS-STING通路来加剧缺血性中风.
METTL14静音表现出神经保护作用,为IS提供了潜在的治疗策略.
这项研究为脑缺血性中风的表观遗传调节提供了新的见解.

关键词:

炎症炎症是一种炎症.微质细胞中的微质细胞在NLRP3炎症酶组中,热性灭症 (Pyroptosis) 是一种 m6A 一个很好的.

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