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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 |
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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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Received: 15 October 2023
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