| First Author | Wang T | Year | 2017 |
| Journal | Int J Biol Sci | Volume | 13 |
| Issue | 12 | Pages | 1540-1546 |
| PubMed ID | 29230102 | Mgi Jnum | J:266357 |
| Mgi Id | MGI:6193488 | Doi | 10.7150/ijbs.23000 |
| Citation | Wang T, et al. (2017) Specific Deletion of beta-Catenin in Col2-Expressing Cells Leads to Defects in Epiphyseal Bone. Int J Biol Sci 13(12):1540-1546 |
| abstractText | The role of canonical Wnt/beta-catenin signaling in postnatal bone growth has not been fully defined. In the present studies, we generated beta-catenin conditional knockout (KO) mice and deleted beta-catenin in Col2-expressing chondrocytes and mesenchymal progenitor cells. Findings from analyzing the beta-catenin(Col2CreER) KO mice revealed severe bone destruction and bone loss phenotype in epiphyseal bone, probably due to the increase in osteoclast formation and the accumulation of adipocytes in this area. In addition, we also found bone destruction and bone loss phenotype in vertebral bone in beta-catenin(Col2CreER) KO mice. These findings indicate that beta-catenin signaling plays a critical role in postnatal bone remodeling. Our study provides new insights into the regulation of epiphyseal bone homeostasis at postnatal stage. |
