| First Author | Candela ME | Year | 2016 |
| Journal | PLoS One | Volume | 11 |
| Issue | 6 | Pages | e0156783 |
| PubMed ID | 27280771 | Mgi Jnum | J:252282 |
| Mgi Id | MGI:6094709 | Doi | 10.1371/journal.pone.0156783 |
| Citation | Candela ME, et al. (2016) Alpha 5 Integrin Mediates Osteoarthritic Changes in Mouse Knee Joints. PLoS One 11(6):e0156783 |
| abstractText | Osteoarthritis (OA) is one of most common skeletal disorders and can affect synovial joints such as knee and ankle joints. alpha5 integrin, a major fibronectin receptor, is expressed in articular cartilage and has been demonstrated to play roles in synovial joint development and in the regulation of chondrocyte survival and matrix degradation in articular cartilage. We hypothesized that alpha5 integrin signaling is involved in pathogenesis of OA. To test this, we generated compound mice that conditionally ablate alpha5 integrin in the synovial joints using the Gdf5Cre system. The compound mice were born normally and had an overall appearance similar to the control mice. However, when the mutant mice received the OA surgery, they showed stronger resistance to osteoarthritic changes than the control. Specifically the mutant knee joints presented lower levels of cartilage matrix and structure loss and synovial changes and showed stronger biomechanical properties than the control knee joints. These findings indicate that alpha5 integrin may not be essential for synovial joint development but play a causative role in induction of osteoarthritic changes. |
