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首页> 外文期刊>Developmental cell >KIf2 is an essential regulator of vascular hemodynamic forces in vivo
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KIf2 is an essential regulator of vascular hemodynamic forces in vivo

机译：KIf2是体内血管血液动力的重要调节剂

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摘要

Hemodynamic responses that control blood pressure and the distribution of blood flow to different organs are essential for survival. Shear forces generated by blood flow regulate hemodynamic responses, but the molecular and genetic basis for such regulation is not known. The transcription factor KLF2 is activated by fluid shear stress in cultured enclothelial cells, where it regulates a large number of vasoactive endothelial genes. Here, we show that KIf2 expression during development mirrors the rise of fluid shear forces, and that enclothelial loss of KIf2 results in lethal embryonic heart failure due to a high-cardiac-output state. KIf2 deficiency does not result in anemia or structural vascular defects, and it can be rescued by administration of phenylephrine, a catecholamine that raises vessel tone. These findings identify KIf2 as an essential hemodynamic regulator in vivo and suggest that hemodynamic regulation in response to fluid shear stress is required for cardiovascular development and function.
机译：控制血压和血流向不同器官的分布的血液动力学反应对于生存至关重要。由血流产生的剪切力调节血液动力学响应，但是尚不清楚这种调节的分子和遗传基础。转录因子KLF2在培养的内皮细胞中被流体剪切应力激活，在其中调节大量的血管活性内皮基因。在这里，我们显示了在发育过程中KIf2的表达反映了流体剪切力的上升，而KIf2的覆盖丢失导致由于高心输出量而致死的胚胎性心力衰竭。 KIf2缺乏症不会导致贫血或血管结构缺陷，可以通过服用苯肾上腺素（一种增加血管张力的儿茶酚胺）来挽救它。这些发现将KIf2鉴定为体内必不可少的血液动力学调节剂，并表明响应流体剪切应力的血液动力学调节是心血管发展和功能所必需的。

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