Ando J, Komatsuda T, Kamiya A
Research Institute of Applied Electricity, Hokkaido University, Sapporo, Japan.
In Vitro Cell Dev Biol. 1988 Sep;24(9):871-7. doi: 10.1007/BF02623896.
Vascular endothelial cells modulate their structure and functions in response to changes in hemodynamic forces such as fluid shear stress. We have studied how endothelial cells perceive the shearing force generated by blood flow and the substance(s) that may mediate such a response. We identify cytoplasmic-free calcium ion (Ca++), a major component of an internal signaling system, as a mediator of the cellular response to fluid shear stress. Cultured monolayers of bovine aortic endothelial cells loaded with the highly fluorescent Ca++-sensitive dye Fura 2 were exposed to different levels of fluid shear stress in a specially designed flow chamber, and simultaneous changes in fluorescence intensity, reflecting the intracellular-free calcium concentration [( Ca++]i), were monitored by photometric fluorescence microscopy. Application of shear stress to cells by fluid perfusion led to an immediate severalfold increase in fluorescence within 1 min, followed by a rapid decline for about 5 min, and finally a plateau somewhat higher than control levels during the entire period of the stress application. Repeated application of the stress induced similar peak and plateau levels of [Ca++]i but at reduced magnitudes of response. These responses were observed even in Ca++-free medium. Thus, a shear stress transducer might exist in endothelial cells, which perceives the shearing force on the membrane as a stimulus and mediates the signal to increase cytosolic free Ca++.
血管内皮细胞会根据诸如流体剪切应力等血流动力学力的变化来调节其结构和功能。我们研究了内皮细胞如何感知由血流产生的剪切力以及可能介导这种反应的物质。我们确定细胞质游离钙离子(Ca++),一种内部信号系统的主要成分,作为细胞对流体剪切应力反应的介质。将装载有高荧光Ca++敏感染料Fura 2的牛主动脉内皮细胞培养单层置于专门设计的流动腔室中,暴露于不同水平的流体剪切应力下,通过光度荧光显微镜监测反映细胞内游离钙浓度[(Ca++)i]的荧光强度的同时变化。通过流体灌注对细胞施加剪切应力导致1分钟内荧光立即增加几倍,随后快速下降约5分钟,最后在整个应力施加期间达到略高于对照水平的平台期。重复施加应力会诱导类似的[Ca++]i峰值和平台期水平,但反应幅度降低。即使在无Ca++的培养基中也观察到这些反应。因此,内皮细胞中可能存在一种剪切应力传感器,它将膜上的剪切力感知为一种刺激,并介导信号以增加胞质游离Ca++。