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

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.

journal_name

J Cell Physiol

authors

Xia C,Wang P,Fang L,Ge Q,Zou Z,Dong R,Zhang P,Shi Z,Xu R,Zhang L,Luo C,Ying J,Xiao L,Shen J,Chen D,Tong P,Jin H

doi

10.1002/jcp.28491

subject

Has Abstract

pub_date

2019-08-01 00:00:00

pages

18535-18543

issue

10

eissn

0021-9541

issn

1097-4652

journal_volume

234

pub_type

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