血管光滑肌细胞在血管炎症的3细胞模型中增强了免疫/血管相互作用

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Updated: Jul 15, 2025

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A Cell Culture Model of Resistance Arteries

Published on: September 8, 2017

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Jolanta Wiejak¹, Fiona A Murphy², Pasquale Maffia^3,4,5

¹Institute of Biological Chemistry, Biophysics and Bioengineering, Heriot-Watt University, Edinburgh, EH14 4AS, UK.

Scientific reports

|September 23, 2023

概括

血管光滑肌细胞 (VSMCs) 在与巨细胞相互作用时显著放大内皮细胞的炎症反应. 这一发现表明,三细胞模型对于研究动脉样硬化发展和潜在治疗方法至关重要.

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
细胞生物学细胞生物学

背景情况:

动脉样硬化涉及慢性炎症和动脉中的斑块积累.
这个过程是由血管光滑肌细胞 (VSMC),血管内皮细胞 (VEC) 和巨细胞 (Ms) 之间的复杂相互作用驱动的.
由于它们的可塑性,VSMC在动脉瘤的发展中具有双重作用.

研究的目的:

研究VSMCs在调节VECs的细胞因子/化学因子配置和基因表达中的作用.
了解VSMCs如何影响人体血管炎症模型中VECs对激活巨细胞的反应.
评估三细胞共同培养系统适用于研究免疫和血管细胞交叉的适用性.

主要方法:

使用人类冠状动脉内皮细胞 (HCAECs),THP1巨细胞和VSMCs开发一个三细胞共同培养模型.
用脂聚糖 (LPS) 刺激巨细胞.
在HCAEC中分析细胞因子产生和炎症基因表达.

主要成果:

在与LPS刺激的THP1 Ms共培养的HCAEC中,VSMCs的存在显著增强了细胞因子 (CXCL1/GROα,IL-6,IL-8,CCL2/MCP1) 的产生.
VSMC导致HCAEC炎症基因的上调,包括那些参与JAK/STAT,Jun和NFκB信号通路的炎症基因.
这些结果表明,VSMCs在免疫内皮细胞交叉交谈中发挥着关键作用.

结论:

大型肌肉细胞是免疫和内皮细胞之间的炎症相互作用的重要调解者.
与两细胞模型相比,三细胞共同培养模型提供了更准确的血管炎症表示.
研究结果表明,针对VSMC相互作用可能是动脉样硬化治疗的治疗策略.

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