NAT10通过调节ac4C修改TLR9调节由巨细胞极化介导的动脉样硬化进展
Wei Yin1, Jie Wang1, Lingling Li1
1Department of Cardiology, Suzhou Research Center of Medical School, Suzhou Hospital, Affiliated Hospital of Medical School, Nanjing University, No.1 Lijiang Road, High-Tech Zone, Suzhou, 215153, China.
Journal of cardiovascular translational research
|December 19, 2024
概括
N-乙转移酶10 (NAT10) 通过通过N4-乙细胞素 (ac4C) 修改TLR9.9改变巨细胞极化来调节动脉样硬化. 这一发现为治疗这种炎症性疾病提供了新的见解.
科学领域:
- 心血管研究研究心血管研究
- 免疫学 免疫学 免疫学
- 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:
- 动脉样硬化 (AS) 是一种由巨细胞两极分化驱动的炎症状况.
- 由N-乙转移酶10 (NAT10) 介导的N4-乙细胞酶 (ac4C) 修饰在细胞过程中起作用.
研究的目的:
- 在AS.的背景下调查ac4C修饰在巨分化中的作用.
- 阐明NAT10影响AS进展的机制.
主要方法:
- 进行了体内和体外实验.
- 使用点点的方法量化了ac4C水平.
- 通过定量实时PCR和流细胞测量来评估巨细胞极化.
- 通过甲基化RNA免疫沉 (MeRIP),RIP和双 luciferase 记者测定来探索机制.
主要成果:
- 在AS患者中观察到增加NAT10表达和ac4C水平.
- NAT10的淘汰促进了M1到M2的巨细胞两极分化,并降低了TLR9的ac4C水平.
- 过度表达TLR9可以抵消NAT10对巨细胞两极分化的影响.
- 在体内,NAT10倒置抑制了M1极化和AS进展.
结论:
- NAT10通过调节巨细胞极化来调节AS的进展.
- 这种调节通过控制TLR9.9的ac4C修改来实现.
- 这项研究为AS治疗策略提供了新的理论基础.
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