Dual effect of fluid shear stress on volume-regulated anion current in bovine aortic endothelial cells.
Dual effect of fluid shear stress on volume-regulated anion current in bovine aortic endothelial cells.
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流体剪切应力对牛主动脉内皮细胞体积调节阴离子电流的双重影响。
DOI：
10.1152/ajpcell.00247.2001
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
Levitan,Irena
中科院分区：
文献类型：
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作者：
Romanenko,VictorG;Davies,PeterF;Levitan,Irena
维持细胞体积稳态的关键机制是激活体积调节阴离子电流（VRAC）。研究了血流动力学剪切应力对牛主动脉内皮细胞VRAC的调节作用。我们发现剪应力的急剧变化对VRAC的发展有双相影响。从背景流量（0.1 dyn/cm2）到1 dyn/cm2的剪切应力步骤增强了渗透挑战诱导的VRAC激活。在没有渗透胁迫的情况下，单独流动不会诱导VRAC激活。然而，将剪切应力增加到3 dyn/cm2时，VRAC活性只会短暂增加，随后进入抑制期，在此期间VRAC活性逐渐被抑制。当剪应力进一步增大（5-10 dyn/cm2）时，电流立即被强烈抑制。在渗透挑战的细胞和在等渗条件下自发VRAC的细胞中都观察到VRAC的抑制。我们的研究结果表明，剪切应力是调节血管内皮细胞维持体积稳态能力的一个重要因素。
The key mechanism responsible for maintaining cell volume homeostasis is activation of volume-regulated anion current (VRAC). The role of hemodynamic shear stress in the regulation of VRAC in bovine aortic endothelial cells was investigated. We showed that acute changes in shear stress have a biphasic effect on the development of VRAC. A shear stress step from a background flow (0.1 dyn/cm2) to 1 dyn/cm2enhanced VRAC activation induced by an osmotic challenge. Flow alone, in the absence of osmotic stress, did not induce VRAC activation. Increasing the shear stress to 3 dyn/cm2, however, resulted in only a transient increase of VRAC activity followed by an inhibitory phase during which VRAC was gradually suppressed. When shear stress was increased further (5–10 dyn/cm2), the current was immediately strongly suppressed. Suppression of VRAC was observed both in cells challenged osmotically and in cells that developed spontaneous VRAC under isotonic conditions. Our findings suggest that shear stress is an important factor in regulating the ability of vascular endothelial cells to maintain volume homeostasis.