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ADAR1调节巨细胞的两极分化,并对肝脏缺血和反损伤有保护作用

Linxiao Wang¹, Chujun Duan², Xiuhua Wu³

¹Department of Emergency, Xijing Hospital, Air Force Medical University, Xi'an, China; College of Life Sciences, Northwest University, Xi'an, China.

|December 19, 2023

概括

作用于RNA 1 (ADAR1) 的腺氨酸脱氨酶通过促进抗炎M2巨细胞两极分化,防止肝脏缺血和反损伤 (LIRI). 补充ADAR1可以缓解LIRI病理,并增强肝脏巨细胞的功能.

科学领域:

免疫学免疫学免疫学
肝病学肝病学是一种肝病学.
分子生物学分子生物学

背景情况:

肝脏缺血和再注射损伤 (LIRI) 显著影响肝移植的结果.
基于LIRI的分子机制是复杂的,涉及各种细胞组件.
众所周知,作用于RNA 1 (ADAR1) 的腺氨酸脱氨酶在其他环境中调节巨细胞两极分化.

研究的目的:

在LIRI期间调查ADAR1在肝脏巨细胞中的作用.
探索ADAR1作为LIRI治疗点的潜力.

主要方法:

使用LIRI的小鼠模型和RAW264.7巨细胞的体外低氧-重氧化 (HR) 治疗.
评估了ADAR1表达水平,巨细胞极化标记物和炎症性细胞因子概况.
通过补充和敲击/过度表达操纵ADAR1水平.

主要成果:

诱导LIRI导致ADAR1的表达减少,并改变了肝脏巨细胞的两极分化.
补充ADAR1减轻了LIRI诱导的病理损伤,并促进了M2巨细胞的激活.
低氧降低了ADAR1的表达;ADAR1的过度表达增强了抗炎细胞因子的产生和HR条件下的M2极化.
抑制ADAR1可以逆转这些影响.

结论:

ADAR1促进肝脏巨细胞的M2两极化,提供对LIRI的保护作用.
ADAR1代表了一种新的治疗点,用于预防和治疗肝脏缺血和再注射损伤.

关键词:

在 ADAR1 中,ADAR1 是缺氧和重新氧化的情况.缺血和反伤害的伤害肝脏肝脏肝脏肝脏巨细胞是一个巨细胞.

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