层状剪切应力上调补充抑制蛋白质集群蛋白:一种新的强有力的防御机制,对补充诱导的内皮细胞激活
C Urbich1, M Fritzenwanger, A M Zeiher
1Molecular Cardiology, Department of Internal Medicine IV, University of Frankfurt, Germany.
Circulation
|February 2, 2000
概括
剪切应激通过增加保护性蛋白质集群蛋白来减少内皮细胞中补充诱导的炎症. 这一发现可能解释了剪切应力如何防止动脉样硬化发展.
科学领域:
- 心血管生物学 心血管生物学
- 免疫学 免疫学 免疫学
- 内皮细胞生物学 内皮细胞生物学
背景情况:
- 补体系统有助于动脉样硬化病原.
- 在内皮细胞 (ECs) 中的补充激活会触发一种前炎性反应.
- 生理剪切应激具有保护性抗动脉样硬化作用.
研究的目的:
- 为了研究剪切应力是否对抗补充介导的EC激活.
- 阐明剪切应力的保护作用背后的分子机制.
主要方法:
- ECs被暴露在补充血清 (CS) 上,有或没有先前的层状剪切应力.
- 量化了炎症标记物 (IL-8,MCP-1) 和聚类蛋白的mRNA和蛋白质表达.
- 通过使用反感性寡核酸和过度表达,评估了聚类蛋白功能.
主要成果:
- 在ECs中补充血清上调的IL-8和MCP-1mRNA.
- 层切割应力取消了CS诱导的IL-8释放,并减少了MCP-1的表达.
- 剪切应激增加了mRNA和蛋白质水平中的集群.
- 集群蛋白抑制逆转了剪切应力的保护作用,而过度表达抑制了EC激活.
结论:
- 剪切应力通过对集群蛋白进行上调来防止补充诱导的EC炎症.
- 由于剪切应力增加集群蛋白表达,可以通过抑制ECs上的补体激活来预防动脉样硬化.
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