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Activation of β‐catenin in Col2 ‐expressing chondrocytes leads to osteoarthritis‐like defects in hip joint
Author(s) -
Xia Chenjie,
Wang Pinger,
Fang Liang,
Ge Qinwen,
Zou Zhen,
Dong Rui,
Zhang Peng,
Shi Zhenyu,
Xu Rui,
Zhang Lei,
Luo Chen,
Ying Jun,
Xiao Luwei,
Shen Jie,
Chen Di,
Tong Peijian,
Jin Hongting
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28491
Subject(s) - osteoarthritis , pathogenesis , femoral head , chondrocyte , cartilage , phenotype , catenin , medicine , pathological , pathology , degenerative disease , disease , gene , anatomy , microbiology and biotechnology , signal transduction , biology , wnt signaling pathway , genetics , alternative medicine
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.