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Vol. 65 No. 4: Issue 4

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Lipopolysaccharide pretreatment inhibits oxidative stress-induced endothelial progenitor cell apoptosis via a TLR4-mediated PI3K/Akt/ NF-κB p65 signaling pathway

https://doi.org/10.14715/cmb/2019.65.4.17
Meihui Wang
Department of Cardiology, Biomedical Research (Therapy) Center, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310016, P.R. China
Liang Xia
Department of Cardiology, Biomedical Research (Therapy) Center, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310016, P.R. China
Guosheng Fu
Department of Cardiology, Biomedical Research (Therapy) Center, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310016, P.R. China

Corresponding Author(s) : Guosheng Fu

awuvw9@163.com

Cellular and Molecular Biology, Vol. 65 No. 4: Issue 4

Abstract

Endothelial progenitor cells (EPCs) improve neovascularization and endothelium regeneration. Transplantation with EPCs is a therapeutic strategy for the treatment of ischemic diseases. However, the transplanted EPCs are susceptible to adverse environments such as hypoxia, inflammation and oxidative stress. Oxidative stress-induced apoptosis of transplanted EPCs greatly reduces their therapeutic efficacy. Lipopolysaccharide (LPS) is a highly immunogenic antigen. Recent findings suggest that low dose of LPS pretreatment has protective effect against apoptosis. In this study, the role of LPS in apoptosis of EPCs was investigated. Pretreatment with 1µg/ml LPS prevented oxidative stress-induced EPCs apoptosis and ROS generation, which effects were abolished by TAK-242, a specific TLR4 antagonist. Further investigation of the mechanisms demonstrated that the activation was mediated by TLR4, and that PI3K/Akt/ NF-κB p65 signaling pathway may play a critical role in the process.

Keywords

Endothelial progenitor cells Lipopolysaccharide Oxidative stress Toll-like receptors 4.
Wang, M., Xia, L., & Fu, G. (2019). Lipopolysaccharide pretreatment inhibits oxidative stress-induced endothelial progenitor cell apoptosis via a TLR4-mediated PI3K/Akt/ NF-κB p65 signaling pathway. Cellular and Molecular Biology, 65(4), 101–106. https://doi.org/10.14715/cmb/2019.65.4.17
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