Angiopoietin-like protein 7 mediates TNF-α-induced adhesion and oxidative stress in human umbilical vein epithelial cells
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.