在流量条件下,MCP-1和IL-8触发单细胞与血管内皮的坚固粘附
R E Gerszten1, E A Garcia-Zepeda, Y C Lim
1The Cardiovascular Research Center and Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston 02114, USA.
Nature
|May 5, 1999
概括
单细胞化学吸引蛋白-1 (MCP-1) 和互白素-8 (IL-8) 化学基因促进单细胞粘附于血管内皮. 这项研究揭示了IL-8的存在
科学领域:
- 免疫学 免疫学 免疫学
- 心血管生物学 心血管生物学
- 细胞和分子医学 细胞和分子医学
背景情况:
- 单细胞是动脉样硬化发展的关键参与者.
- 化学因子单细胞化学吸引蛋白-1 (MCP-1) 和介质素-8 (IL-8) 涉及到动脉瘤.
- 对于IL-8在单细胞招募到血管病变中的确切作用尚不清楚.
研究的目的:
- 在流动条件下,研究化基因在控制单细胞与血管内皮相互作用中的作用.
- 确定MCP-1和IL-8是否可以诱导单细胞与表达E-selectin的内皮细胞的坚固粘附.
- 阐明化基因调节单细胞-内皮细胞相互作用的机制.
主要方法:
- 在流动条件下研究单细胞-内皮细胞相互作用.
- 使用血管内皮被转化以表达特定的白细胞粘附受体,包括E-selectin.
- 评估MCP-1和IL-8对单细胞粘附,过渡物和化学反应的影响.
主要成果:
- 无论是MCP-1还是IL-8,都迅速诱导滚动单细胞对表达E-选择素的内皮单层的坚固粘附.
- 这些促进粘附的效应与与之相关的化学激素不同,是MCP-1和IL-8的特征.
- 观察到的坚固粘附与过渡性或化学反应诱导无关.
结论:
- 化学因子,包括IL-8,是流动下单细胞-内皮细胞相互作用的显著调节器.
- IL-8在触发固体单细胞对血管内皮的粘附方面发挥了以前未知的强大作用.
- 这些发现为血管炎症和动脉样硬化中单细胞招募机制提供了新的见解.
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