Laminar shear stress is considered to improve endothelial cell (EC) function. However, the underlying mechanism is unclear. Autophagy has been found to protect cell survival under stress. In this study, the effect of laminar shear stress on EC autophagy and its potential mechanism were explored. The autophagic markers, Beclin 1 and LC3 II, in human umbilical vascular endothelial cells increased after laminar shear stress treatment. Meanwhile, the autophagic substrate, p62, decreased. The protein level of Rab4 increased under laminar shear stress. When pretreated with Rab4 siRNA, the increased levels of Beclin 1 and LC3 II were attenuated and p62 levels significantly increased. In addition, the MCP level and the adhesion of monocytes were also obviously increased by Rab4 siRNA. Laminar shear stress upregulated Rab4 expression, which contributed to improved EC autophagy and function.
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