Home HOME General Physiology and Biophysics 2020 General Physiology and Biophysics Vol.39, No.3, p.285–292, 2020

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Quarterly, 80 pp. per issue
Founded: 1982
ISSN  1338-4325 (online)

Published in English

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General Physiology and Biophysics Vol.39, No.3, p.285–292, 2020

Title: Angiopoietin-like protein 7 mediates TNF-α-induced adhesion and oxidative stress in human umbilical vein epithelial cells
Author: Jiong Li, Tianxiang Liang, Yanzheng Wang, Yirong Gan, Zongke Kou, Yunlong Zhang, Rui Mao, Dingxiong Xie

Abstract: Tumor necrosis factor-α (TNF-α) promotes monocyte adhesion to endothelium and accumulation of endothelium will lead to atherosclerosis. The present study explored angiopoietin-like protein (Angptl7) as a potential target in the process of atherosclerosis, and its role in the adhesion and oxidative stress induced by TNF-α in human umbilical vein epithelial cells (HUVEC). The initiation of atherosclerosis is endothelial injury. Angptl7 was dramatically increased in TNF-α-induced HUVEC compared to the control cells. After Angptl7 effectively knocked-down in TNF-α-induced HUVEC, the levels of reactive oxygen species (ROS), interleukin (IL)-1β, IL-6 and cyclooxygenase-2 (Cox-2) were prominently decreased, whereas the levels of nitric oxide (NO) and endothelia nitric oxide synthase (eNOS) were increased. Inhibition of Angptl7 significantly reversed TNF-α-induced cell adhesion in HUVEC. Finally, downregulation of Angptl7 significantly reduced the expression of nuclear factor-κB (NF-κB) and enhanced the levels of nuclear factor erythroid 2-related factor 2 (Nrf-2) and heme oxygenase-1 (HO-1) in TNF-α-treated HUVEC. Angptl7 conducted TNF-α-induced oxidative stress and cell adhesion in HUVEC. Therefore, Angptl7 might participate in the development of endothelial injury and further atherosclerosis. This might give us a new insight for investigation of procession of atherosclerosis.

Keywords: Angiopoietin-like protein 7, Atherosclerosis, Cell adhesion, Oxidative stress, Inflammation
Published online: 10-Jun-2020
Year: 2020, Volume: 39, Issue: 3 Page From: 285, Page To: 292

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