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基于实验的计算模型预测,IL-6经典和转信号在诱导内皮细胞下游信号中表现出类似的效能

Min Song¹, Youli Wang², Brian H Annex²

¹Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. msong25@jhmi.edu.

NPJ systems biology and applications

|September 21, 2023

概括

在内皮细胞中介质素-6 (IL-6) 信号传递是为了理解炎症和血管生成而建模的. 该模型揭示了跨信号是主要的,为向治疗提供了洞察力.

科学领域:

计算生物学和系统医学计算机生物学和系统医学
分子和细胞生物学分子和细胞生物学
免疫学和炎症研究研究.

背景情况:

炎症性细胞因子,比如INTERLEUKIN-6 (IL-6),与血管生成相关的疾病有关.
针对血管新生已经显示出有限的成功,可能是由于炎症和血管新生之间的相互作用.
了解内皮细胞中的IL-6信号传递至关重要,但尚未完全阐明.

研究的目的:

在内皮细胞中开发IL-6经典和跨信号通路的计算模型.
量化描述关键下游信号分子的动态:酸化的STAT3 (pSTAT3),Akt (pAkt) 和ERK (pERK).
为了确定IL-6介导的炎症和血管新生信号的关键调节器.

主要方法:

开发一个详细的,基于实验的IL-6信号的计算模型.
对IL-6对STAT3,PI3K/Akt和MAPK通路的经典和转信号影响的定量表征.
模型验证和应用以预测信号动态和识别有影响力的参数.

主要成果:

IL-6的经典和跨信号反应是依赖IL-6和可溶性IL-6受体 (sIL-6R) 的剂量.
转信号表现出更强的下游反应,并因大量的sIL-6R而在体外主导IL-6效应.
两种IL-6和sIL-6R水平都调节信号强度,特定的物种和参数被确定为关键调节器.

结论:

计算模型量化预测IL-6在内皮细胞中的经典和跨信号效应.
该模型为整合实验数据和理解IL-6介导炎症和血管生成提供了一个框架.
这种方法可以指导识别用于调节内皮细胞IL-6信号传递的新型治疗点.

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