Platelet-rich plasma protects HUVECs against oX-LDL-induced injury

Author:

Wang Yang1,Wang Jinsong1,Li Yonghui1,Wang Shenming1,Zhu Xiaonan2

Affiliation:

1. First Affiliated Hospital of Sun Yat-Sen University , GuangZhou , GuangDong , China

2. Sun Yat-sen University Zhongshan School of Medicine , GuangZhou , China

Abstract

Abstract Platelet-rich plasma (PRP) contains a variety of cytokines, some of which ameliorate oX-LDL (oxidized low-density lipoprotein)-induced endothelial cell (EC) injury. Therefore, we hypothesized that PRP might alleviate oX-LDL-induced injury. Methodology Human umbilical vein endothelial cells (HUVECs) were divided into four groups: a PPP (platelet-poor plasma) group, an oX-LDL group, an oX-LDL+PRP group and a PRP group. CCK-8 (Cell Counting Kit) assay, Annexin V-FITC/7-AAD and Hochest 33342 staining were performed to assess cell proliferation and apoptosis. Tube formation and cell migration assays were performed to evaluate HUVEC-mediated vasculogenesis and migration. Expression levels of Bcl-2, Bax, caspase-3, cleaved caspase-3, PI3K, Akt, eNOS p-Akt, p-eNOS, IL-6 and IL-1 were detected by western blotting or immunofluorescence. Principal findings PRP promoted HUVEC proliferation in a non-linear pattern, protected HUVECs against oX-LDL-induced apoptosis and attenuated oX-LDL-mediated inhibition of HUVEC migration and vasculogenesis. Additionally, compared to the PPP group, PRP downregulated pro-apoptotic proteins (ratio of Bax/Bcl-2, caspase-3 and cleaved caspase-3) as well as IL-6 and IL-1. Moreover, the PI3K/Akt/eNOS pathway was activated by PRP and inactivated by oX-LDL. Conclusions It was demonstrated that PRP protected HUVECs against oX-LDL-induced injury and that the PI3K/Akt/eNOS pathway was activated in this process.

Publisher

Walter de Gruyter GmbH

Subject

General Medicine

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