| First Author | Xia C | Year | 2019 |
| Journal | J Cell Physiol | Volume | 234 |
| Issue | 10 | Pages | 18535-18543 |
| PubMed ID | 30912140 | Mgi Jnum | J:290750 |
| Mgi Id | MGI:6442633 | Doi | 10.1002/jcp.28491 |
| Citation | Xia C, et al. (2019) Activation of beta-catenin in Col2-expressing chondrocytes leads to osteoarthritis-like defects in hip joint. J Cell Physiol 234(10):18535-18543 |
| abstractText | 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 beta-catenin plays a critical role in hip OA pathogenesis. Here, we showed overexpressed beta-catenin protein in human OA cartilage tissues. Then, we analyzed beta-cat(ex3)(Col2ER) mice, in which beta-catenin gene was conditionally activated in femoral head chondrocytes. At 2 months of age, beta-cat(ex3)(Col2ER) mice already showed a phenotype of severe cartilage degeneration in the femoral head. More changes observed in beta-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 beta-catenin activation possibly contributed to this hip OA-like phenotype. Overall our findings provide direct evidence about the importance of beta-catenin in hip OA pathogenesis. |
