Activation of β-catenin in Col2-expressing chondrocytes leads to osteoarthritis-like defects in hip joint

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

Research output: Contribution to journalArticlepeer-review

9 Scopus citations


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.

Original languageEnglish
Pages (from-to)18535-18543
Number of pages9
JournalJournal of Cellular Physiology
Issue number10
StatePublished - Oct 2019


  • apoptosis
  • cartilage degeneration
  • hip joint
  • osteoarthritis
  • β-catenin


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