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- Shao-Fei Yu, Wan-Yu Feng, Shao-Qing Chai, Xiao-Bo Meng, Zhong-Xia Dou, and Hua Zhu.
- Department of Pediatrics, Inner Mongolia People's Hospital, Huhhot, Inner Mongolia, China. Electronic address: yushaofei0707@163.com.
- Am. J. Med. Sci. 2018 Jul 1; 356 (1): 64-71.
BackgroundApoptosis of human umbilical vein endothelial cells (HUVECs) plays an important role in the progression of Henoch-Schonlein purpura (HSP). In the present study, we explored the function of miR-218-5p in HUVEC apoptosis and HSP development.Materials And MethodsHSP rat model was established and peripheral blood mononuclear cells (PBMC) were isolated. The expression of miR-218-5p and high-mobility group box-1 (HMGB1) protein in HUVECs was determined by quantitative real-time polymerase chain reaction and western blot, respectively. Cell apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling assay. The association between miR-218-5p and HMGB1 was determined by luciferase assay. The endogenous expression of related genes was modulated with recombinant plasmids and cell transfection.ResultsMiR-218-5p was down-regulated and HMGB1 was up-regulated in vessels of the lower limb of HSP rats and in HUVECs co-cultured in HSP PBMC supernatant. MiR-218-5p negatively regulated HMGB1 by targeting its 3'-untranslated regions. Over expression of miR-218-5p reversed the increased apoptosis and HMGB1 expression observed in HUVECs co-cultured in PBMC supernatant, whereas miR-218-5p knockdown showed the opposite outcomes. Furthermore, the miR-218-5p mimic demonstrated an inhibitory effect on the apoptosis of HUVECs co-cultured in PBMC supernatant, which was reversed by over expression of HMGB1. In HSP rats, over expression of miR-218-5p attenuated HSP and decreased the level of HMGB1.ConclusionsMiR-218-5p attenuated HSP at least partly through regulating HMGB1 expression and affecting the function of HUVECs.Copyright © 2018 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.
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