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在高胆固醇血症小鼠中,痕信号调节了动脉损伤恢复期间的内皮原生细胞活性
Masaaki Ii1, Kyosuke Takeshita, Kayoko Ibusuki
1Feinberg Cardiovascular Research Institute, Northwestern University, Chicago, IL 60611, USA.
在小鼠中,高胆固醇意外地增强了内皮原生细胞 (EPC) 功能和动脉修复. 胆固醇和Notch1信号通路似乎可以调节动脉样硬化中的EPC活性.
科学领域:
- 心血管生物学 心血管生物学
- 细胞生物学 细胞生物学
- 动脉样硬化研究 动脉样硬化研究
背景情况:
- 在动脉样硬化中,内皮原生细胞 (EPC) 的作用在很大程度上是未知的.
- 这项研究调查了胆固醇对再内皮质化,动脉样硬化发展和动脉损伤后EPC功能的影响.
研究的目的:
- 阐明高胆固醇血症对EPC和血管修复的影响.
- 确定胆固醇影响EPC行为和功能的机制.
主要方法:
- 对高胆固醇血症 (ApoE-/-) 和野生型 (WT) 鼠的比较分析.
- 评估重新内皮质化,EPC计数,增殖,粘附,迁移和亡.
- 基因表达分析 (VEGF,Notch1,eNOS) 和骨髓移植研究.
主要成果:
- 与WT小鼠相比,高胆固醇血症小鼠表现出增强的再内皮质化和更高的循环EPC计数.
- 根据胆固醇度调节的EPC扩散,粘附,迁移和抗亡活性.
- 胆固醇改变了EPC中VEGF,Notch1和eNOS的基因表达,Notch1缺乏提高了EPC活动和恢复.
结论:
- 胆固醇在动脉样硬化期间在调节EPC功能方面发挥着重要的,尽管复杂的作用.
- 在血管损伤和胆固醇代谢的背景下,Notch1信号被认为是EPC活动的关键调节者.
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