• Zhiyong Zhu, Xizhuang Bai, Huisheng Wang, Xi Li, Guoqiang Sun, and Pan Zhang.
• Department of Sports Medicine and Joint Surgery, The People's Hospital of China Medical University, Shenyang, Liaoning, China.
• Arch Med Sci. 2020 Jan 1; 16 (4): 898-906.

IntroductionIn our study we aimed to investigate the mechanism of Wnt inhibitory factor 1 (WIF1) on regulating chondrocyte proliferation and apoptosis via reactive oxygen species (ROS) and the Wnt/βcatenin signaling pathway in osteoarthritis (OA).Material And MethodsOsteoarthritis chondrocytes were treated with interleukin 1β (IL-1β) to simulate an inflammatory condition. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot were applied for detecting WIF1 expression in OA chondrocytes. MTT assay and flow cytometry were carried out to analyze the cell proliferation and apoptosis. Content of ROS was detected using flow cytometry, and activity of the Wnt/βcatenin signaling pathway was detected using immunofluorescence, western blot and luciferase reporter assay. Western blot and enzyme-linked immunosorbent assay (ELISA) were performed to detect the expression of apoptosis-related proteins and secretion of matrix metalloproteinases (MMPs).ResultsWIF1 expression in OA chondrocytes was significantly lower than in normal chondrocytes. After WIF1 cDNA transfection, the aberrantly high ROS level in OA chondrocytes was down-regulated, which led to the increase of proliferation and reduction of apoptosis. The Wnt/βcatenin signaling pathway was suppressed by WIF1 overexpression and the secretion of MMPs was therefore reduced.ConclusionsUp-regulation of WIF1 would promote proliferation and suppress apoptosis of OA chondrocytes through eliminating ROS production and reduce secretion of MMPs via blocking the Wnt/βcatenin signaling pathway.Copyright © 2020 Termedia & Banach.

4 keywords...

hide…