暴露于剪切应力会改变内皮质的粘性. 氧化的作用 氧化的作用
P S Tsao1, N P Lewis, S Alpert
1Section of Vascular Medicine, Stanford University, Calif. 94305-5246, USA.
Circulation
|December 15, 1995
概括
剪切应力通过增加氧化 (NO) 的释放来减少单细胞对内皮细胞的粘附. 这种抗粘附效应迅速发生,在30分钟内发生,并且由NO和前环素介导.
科学领域:
- 心血管生物学 心血管生物学
- 内皮细胞功能 内皮细胞功能
- 血液动力学 血液动力学
背景情况:
- 血流造成的剪切应激刺激内皮细胞 (ECs) 释放氧化 (NO).
- 已知来自内皮的NO可抑制单细胞粘附于血管壁.
- 之前暴露于剪切应力可能会通过增加NO释放来降低单细胞的内皮粘性.
研究的目的:
- 调查假设,先前暴露于剪切应力抑制内皮细胞粘附性单细胞.
- 确定氧化 (NO) 和前环素在这种剪切应力诱导的抑制中的作用.
主要方法:
- 培养的内皮细胞 (牛大动脉,人类大动脉,人类静脉) 被暴露在层状流体流中.
- 在条件介质中测量了氧化 (NO) 和6-基托-前列腺素F1α水平.
- 通过将预先条件化的细胞暴露在THP-1单细胞中来评估内皮细胞的粘附性.
- 使用了NO合成 (尼托-L-氨酸) 和前环素生产 (因多甲) 的抑制剂.
主要成果:
- 层状液流量增加了NO和前环素代谢物积累,以时间依赖的方式.
- 在30分钟内,先前暴露在流量下,将单细胞的内皮粘附性降低了50%.
- 这种抗粘合效应被-L-氨酸和四乙离子阻断,并被NO捐赠者逆转.
- 印美素对单细胞粘附的影响最小,这表明前环素的作用很小.
结论:
- 剪切应力迅速改变单细胞的内皮粘性.
- 主要机制涉及流动刺激的氧化 (NO) 的释放.
- простациклин 的作用较小,这种效应很可能是由于粘附分子的信号传导或激活状态的变化,而不是它们的表达.
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