内皮外体作为一个功能调解者来激活巨细胞
Wenwen Lin1,2,3,4,5, Feng Huang1,2,3,4,5, Yin Yuan1,2,3,4,5
1Department of Geriatric Medicine, Fujian Provincial Hospital, Fuzhou, China.
Frontiers in immunology
|August 14, 2023
概括
炎症的内皮外体 (exo-T) 通过激活MAPK/NF-κB信号通路来促进巨细胞 (Mφ) M1极化,脂质沉积和亡. 这些发现突出了exo-T作为动脉样硬化病变发生的关键媒介.
科学领域:
- 细胞生物学 细胞生物学
- 免疫学 免疫学 免疫学
- 心血管研究研究心血管研究
背景情况:
- 通过外体的细胞间通信在生理和病理过程中至关重要.
- 由内皮细胞 (EC) 衍生的外体介导信息交换,并与动脉样硬化有关.
- 炎症EC外体对巨细胞 (Mφ) 功能的影响尚不清楚.
研究的目的:
- 为了研究瘤亡因子-α (TNF-α) 刺激的ECs (exo-T) 对Mφ功能的外体的影响,在体外.
- 阐明涉及信号通路的潜在分子机制.
主要方法:
- 使用TEM,NTA和西方布洛特对外体 (exo和exo-T) 的表征.
- 通过RT-qPCR,流细胞计和各种测定来评估Mφ偏振,脂质沉积,细胞亡和迁移.
- 微RNA测序 (miRNA-Seq) 和生物信息学分析 (GO,KEGG) 用于识别差异表达的miRNA和目标基因.
- 免疫阻塞用于分析MAPK/NF-κB通路中的蛋白质酸化.
主要成果:
- 标有PKH67的exo/exo-T被Mφ.内部化了.
- exo-T暴露使Mφ偏向M1亚型,增加脂质沉积,并促进亡,但没有显著影响迁移.
- miRNA-Seq确定了104种差异表达的miRNA,其中的目标基因丰富于代谢和MAPK信号通路.
- exo-T治疗增强了MAPK/NF-κB相关蛋白质的酸化.
结论:
- 炎症性内皮外体 (exo-T) 充当影响Mφ行为的功能调解者.
- exo-T可以通过MAPK/NF-κB信号通路激活Mφ.
- 这项研究提供了关于内皮外体在动脉样硬化病理生理学中的作用的见解.
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