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由METTL3介导的TIM1通过依赖IGF2BP2的方式促进巨细胞M1的两极化和炎症

Xianrong Du¹, Yinguang Guo², Xiaoqin Zhao³

¹The Geriatrics Department of Shanxi Provincial People Hospital, Shanxi Medical University, Taiyuan, China.

Journal of biochemical and molecular toxicology

|September 13, 2024

概括

T细胞免疫球蛋白粘素1 (TIM1) 促进M1巨细胞的两极分化和炎症,这对于败血症的发展至关重要. METTL3/IGF2BP2/TIM1轴为败血症提供了一个潜在的治疗点.

科学领域:

免疫学免疫学免疫学
分子生物学分子生物学
病理生理学病理生理学

背景情况:

巨细胞的两极分化和炎症在败血症的发病过程中至关重要.
T细胞免疫球蛋白粘素1 (TIM1) 增强了巨细胞的炎症反应.
目前尚不完全了解TIM1在血症中调节巨细胞极化中的作用.

研究的目的:

在毒症的背景下,研究TIM1在巨细胞极化和炎症中的作用.
阐明涉及METTL3和IGF2BP2.2的潜在分子机制.

主要方法:

在人类细胞系中诱导的巨分化 (M1/M2).
通过qRT-PCR和西欧斑块对TIM1,METTL3和IGF2BP2的表达分析.
通过ELISA和流细胞测量进行细胞因子水平评估 (IL-6,IL-1β,TNF-α).
使用MeRIP试验对TIM1进行m6A甲基化分析.
使用双露西法酶报告员和RIP测试的蛋白质相互作用研究.

主要成果:

TIM1倒置抑制了LPS诱导的M1极化和炎症.
通过m6A修饰,METTL3促进了TIM1表达,由IGF2BP2.2识别.
击败METTL3或IGF2BP2可以抑制M1极化和炎症.
TIM1过度表达挽救了METTL3/IGF2BP2敲击的抑制作用.

结论:

METTL3/IGF2BP2/TIM1轴驱动M1巨细胞的极化和炎症.
这个轴代表了毒症治疗的潜在治疗目标.

关键词:

在IGF2BP2BP2的基础上.在M1极化中,M1极化在METTL3中,METTL3是METTL3的第一个类型.败血症这是一种败血症.时间1 TIM1 m6A 修改的修改

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