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内皮特异性切除连素40通过增加CD73依赖的白细胞粘附来促进动脉样硬化
C E Chadjichristos1, K E L Scheckenbach, T A B van Veen
1Division of Cardiology, Geneva University Hospitals and University of Geneva, Geneva, Switzerland.
Circulation
|December 23, 2009
概括
康尼辛40 (Cx40) 间隙结保持一个非炎症性内皮. 降低Cx40通过增加白细胞粘附来加速动脉样硬化,突出Cx40
科学领域:
- 心血管生物学 心血管生物学
- 内皮细胞生物学 内皮细胞生物学
- 动脉样硬化研究 动脉样硬化研究
背景情况:
- 内皮功能障碍导致动脉样硬化.
- 在动脉生成过程中,Connexin40 (Cx40) 的表达减少.
- 在动脉样硬化发展中Cx40的作用需要研究.
研究的目的:
- 为了确定Cx40是否有助于动脉样硬化.
- 研究Cx40影响内皮功能的机制.
主要方法:
- 产生的内皮特异性Cx40删除小鼠 (Cx40del).
- 用高胆固醇饮食来诱导动脉样硬化.
- 评估了动脉样硬化病变的进展和炎症标志物.
- 使用体外方法 (siRNA,反感) 来降低Cx40表达.
主要成果:
- 内皮特异性Cx40删除加速了动脉样硬化进展.
- Cx40del小鼠表现出单细胞透和VCAM-1表达的增加.
- 降低Cx40降低了内皮CD73表达和活性,促进白细胞粘附.
结论:
- 通过Cx40介导的间隙结沟通促进了抗炎性内皮.
- Cx40传播由腺介导的抗炎信号.
- 向Cx40可以增强白细胞的粘附,加速动脉样硬化.
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