Shear stress regulates the endothelial Kir2.1 ion channel
Shear stress regulates the endothelial Kir2.1 ion channel
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DOI：
10.1073/pnas.102184999
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发表时间：
2002-05-28
影响因子：
11.1
通讯作者：
Hoger, A
中科院分区：
文献类型：
--
作者：
Hoger, JH;Ilyin, VI;Hoger, A
内皮细胞（EC）排列在哺乳动物的血管系统中，并对血流产生的流体剪切力（摩擦力）的血液动力学刺激作出反应。当内皮细胞暴露于剪切应力时，最快的反应之一是K+电导的增加，这表明离子通道参与了早期的剪切应力反应。在这里，我们表明，所施加的剪切应力诱导的K+离子电流在细胞表达的内皮Kir2.1通道。该离子电流共享EC中发现的剪切诱导电流的性质。此外，剪切电流诱导可以通过酪氨酸激酶抑制剂特异性地阻止。我们的研究结果确定Kir2.1通道作为内皮剪切反应机制的早期组成部分。
Endothelial cells (ECs) line the mammalian vascular system and respond to the hemodynamic stimulus of fluid shear stress, the frictional force produced by blood flow. When ECs are exposed to shear stress, one of the fastest responses is an increase of K+ conductance, which suggests that ion channels are involved in the early shear stress response. Here we show that an applied shear stress induces a K+ ion current in cells expressing the endothelial Kir2.1 channel. This ion current shares the properties of the shear-induced current found in ECs. In addition, the shear current induction can be specifically prevented by tyrosine kinase inhibition. Our findings identify the Kir2.1 channel as an early component of the endothelial shear response mechanism.