| First Author | Ibaraki K | Year | 2020 |
| Journal | Mol Med Rep | Volume | 21 |
| Issue | 5 | Pages | 2236-2242 |
| PubMed ID | 32186772 | Mgi Jnum | J:317947 |
| Mgi Id | MGI:6835731 | Doi | 10.3892/mmr.2020.11028 |
| Citation | Ibaraki K, et al. (2020) Deletion of p21 expression accelerates cartilage tissue repair via chondrocyte proliferation. Mol Med Rep 21(5):2236-2242 |
| abstractText | Articular cartilage tissue has a poor healing potential, and when subjected to traumatic damage this tissue undergoes cartilage degeneration and osteoarthritis. The association between the regulation of cell cycle checkpoints and tissue regeneration has been previously investigated, and p21 was initially identified as a potent inhibitor of cell cycle progression. However, the effects of p21 defects on damaged tissue remain controversial. Therefore, the aim of the present study was to evaluate the effects of p21 deficiency on cartilage repair. A mouse model of articular cartilage repair was generated by inducing a patellar groove scratch in 8weekold p21knockout (KO) mice and C57Bl/6 wildtype (WT) mice. Mice were sacrificed at 4 and 8 weeks postsurgery. The present study also investigated the effect of p21 deficiency on cartilage differentiation in ATDC5 cells in vitro. Safranin O staining results indicated that cartilage repair initially occurred in p21 KO mice. In addition, immunohistochemical analysis demonstrated that p21 KO upregulated proliferating cell nuclear antigen and increased cell proliferation. However, type II collagen and Sox9 expression levels remained unchanged in p21 KO and WT mice. Moreover, it was identified that p21 downregulation did not affect Sox9 and type II collagen expression levels in vitro. Furthermore, p21 deficiency promoted healing of articular cartilage damage, which was associated with cell proliferation in vivo, and increased chondrocyte proliferation but not differentiation in vitro. Therefore, the present results suggested that p21 does not affect Sox9 or type II collagen expression levels during cartilage differentiation in the repair of cartilage defects. |
