• Sun Minghua, Tian Jiwei, Zhang Lei, Qi Jizhou, Liu Zhiyuan, and Cao Jiangang.
• Department of Orthopaedics, NHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.
• Medicine (Baltimore). 2024 Dec 13; 103 (50): e40676e40676.

AbstractThe object of this study was to propose a Wnt5a-matrix metalloproteinase (MMP)-13 dependent signaling axis for osteoarthritis (OA) progression. To this end, the chondrocytes were isolated from both OA patients and normal controls. The chondrocytes were treated with diverse concentrations of Wnt5a (0, 50, 100, and 200 ng/mL), respectively. The expression levels of Wnt5a, MMP-13, and Collagen type II were examined using reverse transcription-polymerase chain reaction and western blotting. At the same time, the cell proliferation and cell apoptosis of chondrocytes were also observed. Compared with control tissues, the activities of Wnt5a and MMP-13 were significantly enhanced in chondrocytes of OA patients. Treated with different concentrations of Wnt5a (0, 50, 100, and 200 ng/mL), chondrocyte cell proliferation was clearly downregulated. At the same time, the chondrocyte cell apoptosis was obviously accelerated. The expression pattern of Collagen type II was same as cell proliferation manner. Co-treatment of MMP-13 siRNA could significantly compensate the functions of Wnt-5a administration, suggesting MMP-13 was a direct target of Wnt-5a. Collectively, the study speculated a novel Wnt5a-MMP-13 molecular mechanism for OA progression and shed an innovative signaling axis for the disorder.Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.

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