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Circ_0003575 Knockdown通过miR-637/TRAF6轴缓解了动脉样硬化中ox-LDL诱导的人类大动脉内皮细胞功能障碍

Zhanshuai Zhang¹, Shaoqiang Qin¹, Rui Wang¹

¹Department of Cardiovascular Medicine, The First Affiliated Hospital of Hebei North University, Zhangjiakou City, Hebei, China.

Clinical hemorheology and microcirculation

|August 21, 2023

概括

循环RNAcirc_0003575通过破坏人类大动脉内皮细胞促进动脉样硬化. 抑制circ_0003575通过调节miR-637/TRAF6和NF-κB通路来保护这种损伤.

科学领域:

心血管生物学心血管生物学
分子生物学分子生物学
在RNA生物学,RNA生物学.

背景情况:

循环RNAs (circRNAs) 与动脉样硬化 (AS) 的进展有关.
需要阐明circ_0003575在AS病变发生中的特定作用.

研究的目的:

在动脉样硬化的体外模型中研究circ_0003575的功能作用和潜在机制.
确定circ_0003575,microRNA-637 (miR-637) 和TNF受体相关因子6 (TRAF6) 在内皮细胞中的相互作用.

主要方法:

使用氧化低密度脂蛋白 (ox-LDL) 治疗的人类大动脉内皮细胞 (HAECs) 建立了动脉样硬化细胞模型.
评估细胞增殖 (CCK-8,EDU),细胞亡 (流细胞计),血管生成 (管形成试验) 和炎症因子释放 (ELISA).
量化基因和蛋白质表达 (qRT-PCR,西部斑) 和研究的分子相互作用 (双露西法酶,RIP测定).

主要成果:

氧-LDL诱导的内皮细胞损伤,其特征是减少增殖和血管生成,增加亡和炎症.
Knockdown of circ_0003575显著改善了ox-LDL诱导的HAEC损伤. 这是一个非常好的方法.
Circ_0003575直接针对miR-637,这反过来又针对TRAF6.7的目标. MiR-637的过度表达模仿了circ_0003575敲击的保护作用.
Circ_0003575沉默抑制了NF-κB信号通路的激活.

结论:

Circ_0003575 knockdown 对氧-LDL诱导的人类大动脉内皮细胞损伤产生保护作用.
该机制涉及对miR-637/TRAF6轴和NF-κB通路的调节.
Circ_0003575代表了动脉样硬化的潜在治疗标.

关键词:

在 AS AS AS AS AS 里面.在HAECs中,HAECs是最重要的.在TRAF6中,环_000357575 在线观看在线观看在 miR-63737 系统中使用.

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