Nollert M U, Eskin S G, McIntire L V
Biomedical Engineering Laboratory, Rice University, Houston, TX 77251.
Biochem Biophys Res Commun. 1990 Jul 16;170(1):281-7. doi: 10.1016/0006-291x(90)91271-s.
To elucidate some of the early mechanisms underlying the response of primary human endothelial cells to the initiation of flow, we investigated the changes in inositol lipid metabolism in cells exposed to arterial and venous levels of shear stress. We used a radioimmunoassay specific for inositol-1,4,5-trisphosphate (Ins1,4,5P3) to demonstrate that initiation of an arterial shear stress caused a rapid rise in Ins1,4,5P3 levels which peaked after approximately 30 seconds of flow (2.1 +/- 0.2 fold stimulation) and remained elevated for at least 6 minutes after the initiation of flow. This increased Ins1,4,5P3 concentration is similar in magnitude to the increase caused by 10 microM histamine (2.8 +/- 0.3 fold stimulation). Thus these cells may detect the presence of mechanical stress by a signal transduction pathway involving inositol lipid metabolism.
为了阐明原代人内皮细胞对血流启动反应的一些早期机制,我们研究了暴露于动脉和静脉水平剪切应力的细胞中肌醇脂质代谢的变化。我们使用了一种针对肌醇-1,4,5-三磷酸(Ins1,4,5P3)的放射免疫测定法,以证明动脉剪切应力的启动导致Ins1,4,5P3水平迅速升高,在血流开始约30秒后达到峰值(刺激2.1±0.2倍),并在血流启动后至少6分钟内保持升高。这种Ins1,4,5P3浓度的增加幅度与10微摩尔组胺引起的增加相似(刺激2.8±0.3倍)。因此,这些细胞可能通过涉及肌醇脂质代谢的信号转导途径检测机械应力的存在。