揭示磷脂酰丝氨酸在内皮细胞剪切应力介导的保护中的作用。

Julie K Freed, Michael R Shortreed, Christopher J Kleefisch, Lloyd M Smith, Andrew S Greene
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引用次数: 5

摘要

先前的研究表明,暴露于层流剪切应力下的内皮细胞可以免受凋亡刺激,如肿瘤坏死因子(TNF)- α。作者研究了磷脂酰丝氨酸(PS)在这一现象中的作用。Western blot分析裂解的caspase 3作为细胞凋亡的指标,结果显示,在缺乏丝氨酸的情况下,内皮细胞暴露于层流剪切应力下,与在常规培养基中生长的剪切细胞相比,无法抵抗tnf α诱导的细胞凋亡。我们还发现,在不含丝氨酸的细胞中,剪切诱导的Akt通路激活显著降低。此外,使用一种新型同位素标记技术(包括使用福尔马林)对PS进行定量分析显示,剪切处理期间硬脂酰油酸PS(18:0/18:1)没有增加。这些发现表明,基础水平的PS是激活内皮细胞存活途径所必需的,从而有助于剪切应力启动的整体保护机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Revealing the role of phosphatidylserine in shear stress-mediated protection in endothelial cells.

Previous studies have demonstrated that endothelial cells exposed to laminar shear stress are protected from apoptotic stimuli such as tumor necrosis factor (TNF)-alpha. The authors investigated the role of phosphatidylserine (PS) in this phenomenon. Western blot analysis of cleaved caspase 3 was used as an indicator of apoptosis and revealed that in the absence of serine, endothelial cells exposed to laminar shear stress were unable to protect against TNF-alpha-induced apoptosis, in contrast to sheared cells grown in regular medium. It was also found that shear-induced activation of the Akt pathway was significantly decreased in cells grown without serine. In addition, quantitation of PS using a novel isotopic labeling technique involving the use of formalin revealed that stearoyl-oleic PS (18:0/18:1) did not increase during shear treatment. These findings suggest that basal levels of PS are required to activate survival pathways in endothelial cells and thereby contribute to the overall protective mechanism initiated by shear stress.

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