Effect of shear stress on KLF2 and eNOS expression in vein endothelial cells under normal physiology and uremia conditions
10.3760/cma.j.cn121382-20200910-00102
- VernacularTitle:正常生理和尿毒症状态下剪切力对静脉内皮细胞中KLF2及eNOS表达的影响
- Author:
Bingyue WANG
;
Aili JIANG
;
Lan JIA
;
Lihua WANG
- From:
International Journal of Biomedical Engineering
2021;44(1):12-17
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To study the effect of shear stress on the expression of KLF2 and eNOS in venous endothelial cells under physiological and uremic conditions, and to explore the mechanism leading to dysfunction of venous endothelial cells.Methods:Under physiological conditions and uremia conditions, different shear stresses were simulated in the parallel plate flow cavity, and the shear stresses were applied to the venous endothelial cells of each group for 4, 12, and 24 hours. The expression of KLF2 and eNOS was detected by immunohistochemical fluorescent staining technique and real-time fluorescent quantitative PCR technique.Results:Under physiological conditions, KLF2 is obviously regulated by shear stresses. High-intensity shear stresses and physiological shear stresses will up-regulate the expression of KLF2, while low-intensity shear stresses and oscillating shear stresses will down-regulate the expression of KLF2. As the duration of action increases, the expression of KLF2 will also increase. In the state of uremia, the expression of KLF2 is significantly inhibited. Even if high shear stresses is applied, the level of KLF2 is not high-expressed as the physiological state. And under the action of low shear stresses and oscillating shear stresses, KLF2 expression is more significantly inhibited. KLF2 is mainly expressed in the nucleus. With the action of shear stresses, KLF2 is also expressed in the cytoplasm, while eNOS is mainly expressed in granular form in the cytoplasm and nucleus.Conclusions:After arteriovenous fistula operation, the expression of KLF2 and eNOS is inhibited under the action of multiple factors of uremia environment and oscillating shear stresses, which may be the main cause of the occurrence and development of venous endothelial cell dysfunction, intimal hyperplasia, and AVF failure.
