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炎症和正常内皮外体的特征对内皮功能和高血压的发展的影响

Bingwei Li^1,2, Qiuju Zhang^1,2, Rui Yang^1,2

¹Institute of Microcirculation, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100005, China.

|January 19, 2024

概括

炎症外体通过NF-κB促进病态血管生成,而正常外体则支持生理血管生成. 两者都增加了活性氧物种 (ROS),有助于内皮功能障碍和高血压的发展.

科学领域:

心血管生物学心血管生物学
细胞生物学细胞生物学
高血压研究高血压研究

背景情况:

内皮功能障碍是高血压发展的关键因素.
来自内皮细胞的外体细胞可以影响内皮功能和血管生成.
在这些过程中,炎症和正常内皮外体的作用尚未完全阐明.

研究的目的:

研究瘤亡因子-α (TNF-α) 治疗 (炎症性) 和未治疗 (正常) 内皮外体在介导内皮功能和血管生成中的不同作用.
探索潜在的信号通路和反应性氧物种 (ROS) 在外体诱导效应中的参与.
评估这些外体对高血压大鼠模型中的微循环的影响.

主要方法:

从人静脉内皮细胞 (HUVECs) 中分离出外体,使用或不使用TNF-α治疗.
使用激光多普勒成像对自发高血压大鼠 (SHRs) 和WKY大鼠皮肤微循环的体内评估.
在体外分析内皮管形成,血管原蛋白水平,ROS产量,以及关键信号蛋白的西方斑点分析 (STAT3,p38,NF-κB,JNK,Erk).

主要成果:

正常的外体 (C_Exo) 在SHR中增加了血液输液和内皮振荡器振幅.
炎症性 (T_Exo) 和正常的 (C_Exo) 外体促进了内皮管的形成,增加了血管生成因子和ROS.
T_Exo激活了NF-κB和STAT3信号通路,而C_Exo主要增加了STAT3酸化,表明不同的通路参与.

结论:

由TNF-α诱导的外体 (T_Exo) 通过NF-κB通路驱动病态血管生成,导致高血压.
正常的外生体 (C_Exo) 在生理上具有亲血管性作用.
ROS和炎症信号相互作用以调解内皮细胞功能上的外体体效应,影响高血压的发展.

关键词:

内皮质功能障碍内皮质功能障碍外基因组是外基因组的组成部分.这种高血压,高血压.这是一种炎症炎症炎症炎症.有活性氧物种 (ROS).

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