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Activation of β-catenin in Col2-expressing chondrocytes leads to osteoarthritis-like defects in hip joint |
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| Authors: | Chenjie Xia Pinger Wang Liang Fang Qinwen Ge Zhen Zou Rui Dong Peng Zhang Zhenyu Shi Rui Xu Lei Zhang Chen Luo Jun Ying Luwei Xiao Jie Shen Di Chen Peijian Tong Hongting Jin |
| Institution: | 1. Institute of Orthopedics and Traumatology, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China;2. Institute of Orthopedics and Traumatology, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China
The First College of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, China;3. Department of Orthopedic Surgery, Xiaoshan District Hospital of Traditional Chinese Medicine, Hangzhou, China;4. Institute of Orthopedics and Traumatology, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China The First College of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, China Department of Orthopedic Surgery, School of Medicine, Washington University, St. Louis, Missouri;5. Department of Orthopedic Surgery, School of Medicine, Washington University, St. Louis, Missouri;6. Department of Orthopedic Surgery, Rush University Medical Center, Chicago, Illinois;7. Department of Orthopedic Surgery, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China |
| Abstract: | Although osteoarthritis (OA) in the hip joint is a common and debilitating degenerative disease, the precise molecular mechanisms underlying its pathological process remains unclear. This study sets out to investigate whether β-catenin plays a critical role in hip OA pathogenesis. Here, we showed overexpressed β-catenin protein in human OA cartilage tissues. Then, we analyzed β-cat(ex3)Col2ER mice, in which β-catenin gene was conditionally activated in femoral head chondrocytes. At 2 months of age, β-cat(ex3)Col2ER mice already showed a phenotype of severe cartilage degeneration in the femoral head. More changes observed in β-cat(ex3)Col2ER mice with age included subchondral sclerosis and osteophyte formation along joint margins, resembling a hip OA phenotype in humans. In addition, cartilage degradation and chondrocyte apoptosis as the results of β-catenin activation possibly contributed to this hip OA-like phenotype. Overall our findings provide direct evidence about the importance of β-catenin in hip OA pathogenesis. |
| Keywords: | cartilage degeneration β-catenin hip joint osteoarthritis apoptosis |