Protective effect of shearstress on LDL-induced endothelial progenitor cell injury through up-regulation of autophagy
CHEN Lifang1, HUANG Yulang1, CHEN Junyu2, LUO Xinlin2
1. Department of Cardiology, Shenzhen Qianhai Shekou free trade zone hospital, Shenzhen 518067, China; 2. Department of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen 518057, China
Abstract：Objective To analyze the protective mechanism of laminar shear stress (LSS) on endothelial progenitor cells (EPCs) injury induced by oxidized low-density lipoprotein (ox-LDL). Methods The treatment conditions of ox-LDL and LSS in EPCs were analyzed by CCK8. The effects of LSS on the migration and tube formation ability of EPCs before and after treatment with ox-LDL were analyzed by Transwell and tube formation experiments. The effects of LSS and ox-LDL treatment on autophagy and endothelial-mesenchymal transition markers were analyzed by Western blot. The effects of autophagy activators and inhibitors on autophagy and endothelial-mesenchymal transition markers after treatment with ox-LDL and LSS were analyzed by Western blot. Results After treatment with ox-LDL, the proliferation, migration, and tube formation ability of EPCs were down-regulated, and LSS treatment significantly increased them. LSS treatment had a protective effect on ox-LDL-induced EPCs cell injury. In terms of molecular mechanisms, LSS treatment increased the autophagy level of EPCs cells. After treatment with ox-LDL, EPCs cells underwent significant endothelial mesenchymal transition, which was significantly inhibited by LSS treatment. Autophagy activators and inhibitors confirmed these results. Conclusion LSS can inhibit ox-LDL-induced endothelial mesenchymal transformation of EPCs by upregulating autophagy, and plays a protective role in EPCs.
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2024, Vol. 21 
