eISSN: 1896-9151
ISSN: 1734-1922
Archives of Medical Science
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SCImago Journal & Country Rank
4/2020
vol. 16
 
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Osteoporosis
abstract:
Basic research

A study on the mechanism of Wnt inhibitory factor 1 in osteoarthritis

Zhiyong Zhu
1
,
Xizhuang Bai
1
,
Huisheng Wang
1
,
Xi Li
1
,
Guoqiang Sun
1
,
Pan Zhang
1

1.
Department of Sports Medicine and Joint Surgery, The People’s Hospital of China Medical University, Shenyang, Liaoning, China
Arch Med Sci 2020; 16 (4): 898–906
Online publish date: 2020/06/01
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Introduction
In 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/β-catenin signaling pathway in osteoarthritis (OA).

Material and methods
Osteoarthritis 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/β-catenin 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).

Results
WIF1 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/β-catenin signaling pathway was suppressed by WIF1 overexpression and the secretion of MMPs was therefore reduced.

Conclusions
Up-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/β-catenin signaling pathway.

keywords:

osteoarthritis, Wnt inhibitory factor 1, reactive oxygen species, Wnt/β-catenin

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