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Endothelial progenitor cell (EPC) dysfunction is an important physiopathological mechanism in the dynamics of the formation of atherosclerosis. It has been reported that angiotensin II (Ang-II) damages the function of EPCs in atherosclerotic plaque through induction of oxidative stress. Sestrin 2 (Sesn2) serves as an antioxidant role in oxidative stress, however, the exact mechanisms underlying the dynamics of how Sesn2 may factor into EPCs after Ang-II treatments needs to be illustrated. We isolated EPCs from human umbilical cord blood samples and treated with Ang-II. Western blotting, qRT-PCR, transwell assays, immunofluorescence and so on were used to investigate the mechanisms underlying the roles of Sesn2 in EPCs treated with Ang-II. Ang-II was found to promote the apoptosis of EPCs as well as inhibited the mRNA and protein expression of Sesn2. Upregulation of Sesn2 attenuated the negative effect of Ang-II. Sesn2 increased the protein expression of Nrf2 by enhancing P62-dependent autophagy. Silencing of Nrf2 enhanced the degree of apoptosis of EPCs as well as resulted in the impairment of EPC functions through inducing the promotion of (reactive oxygen species) ROS production. Our study results indicated that Sesn2 facilitated the viability of EPCs After treatment with Ang-II, as well as provided a potential therapeutic target to alleviate the progression of atherosclerosis.

Sesn2 attenuates the damage of endothelial progenitor cells induced by angiotensin II through regulating the Keap1/Nrf2 signal pathway