C-反应性蛋白促进单细胞化学吸引蛋白-1 - - 通过调节CC化学因子受体2表达在人体单细胞中的上调调节,促进单细胞化学吸引蛋白-1 - - 介导的化学反应
Ki Hoon Han1, Kyung-Hee Hong, Jae-Hyeong Park
1Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea. steadyhan@amc.seoul.kr
Circulation
|May 12, 2004
概括
C-反应蛋白 (CRP) 直接激活人体单细胞,增加它们的迁移. 这表明升高的CRP可能会驱动动动脉中单细胞的积累,促进动脉样硬化.
科学领域:
- 心血管科学 心血管科学
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- 炎症是动脉样硬化发展的核心因素.
- 升高的C-反应蛋白 (CRP) 预测心血管事件,并可能促进动脉动脉生成.
- 在人类单细胞激活中CRP的直接作用需要进一步研究.
研究的目的:
- 为了确定C反应蛋白 (CRP) 是否直接激活人体循环单细胞.
- 阐明CRP介导的单细胞激活背后的机制.
- 为了将体内CRP水平与单细胞激活标志物相关联.
主要方法:
- 与CRP一起化了THP-1单细胞,以评估CC化学因子受体2 (CCR2) 表达和化学反应.
- 研究了fcgamma受体 (fcgammaR) 的参与和脂酶D1的激活.
- 血清高敏感性CRP水平与人类受试者的单细胞CCR2表达和化学反应相关.
主要成果:
- CRP (10微克/毫升) 显著增加了CCR2表达和单细胞化学吸引蛋白-1 (MCP-1) 介导的化学反应.
- 由CRP诱导的CCR2上调包括FcgammaRI结合和脂酶D1激活.
- 在体内,较高的血清CRP水平与单细胞CR2表达增加和MCP-1-介导的化学反应相关.
结论:
- 较高的C-反应蛋白 (CRP) 直接增强单细胞的化学反应活性.
- CRP可能会促进单细胞在动脉壁中的招募,从而促进动脉动脉产生.
- 这些发现强调了CRP与动脉样硬化的炎症过程之间的直接机械联系.
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