Autophagy Regulates Vascular Endothelial Cell eNOS and ET-1 Expression Induced by Laminar Shear Stress in an Ex Vivo Perfused System
Autophagy Regulates Vascular Endothelial Cell eNOS and ET-1 Expression Induced by Laminar Shear Stress in an Ex Vivo Perfused System
复制标题
自噬调节离体灌注系统中层流剪切应力诱导的血管内皮细胞 eNOS 和 ET-1 表达
DOI：
10.1007/s10439-014-1033-5
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发表时间：
2014-09-01
影响因子：
3.8
通讯作者：
Wang, Gui-xue
中科院分区：
文献类型：
--
作者：
Guo, Fengxia;Li, Xiaohong;Wang, Gui-xue
Vascular endothelial cell function responds to steady laminar shear stress; however, the underlying mechanisms are not fully elucidated. In the present study, we examined the effect of steady laminar shear stress on vascular endothelial cell autophagy and endothelial cell nitric oxide synthase (eNOS) and endothelin-1 (ET-1) expression using an ex vivo perfusion system. Human vascular endothelial cells and common arteries of New Zealand rabbits were pretreated with or without rapamycin or 3-MA for 30 min. These were then placed in an ex vivo cell perfusion system or an ex vivo organ perfusion system under static conditions (0 dynes/cm2) or steady laminar shear stress (5 or 15 dynes/cm2) for 1 h. In both ex vivo perfusion vascular endothelial cells and vascular vessel segment, steady laminar shear stress promoted autophagy and eNOS expression and inhibited ET-1 expression. Compared with steady laminar shear stress treatment alone, the pretreatment of autophagy inducer rapamycin obviously strengthened the expression of eNOS and decreased the expression of ET-1 in both the 5 and 15 dynes/cm2 treatment groups. Moreover, when pretreated with the autophagy inhibitor 3-MA, the eNOS expression was obviously inhibited and the ET-1 expression was reversed. These findings demonstrate that autophagy is upregulated under steady laminar shear stress, improving endothelial cell maintenance of vascular tone function.
