| First Author | Julien A | Year | 2020 |
| Journal | Stem Cell Reports | Volume | 15 |
| Issue | 4 | Pages | 955-967 |
| PubMed ID | 32916123 | Mgi Jnum | J:310477 |
| Mgi Id | MGI:6762770 | Doi | 10.1016/j.stemcr.2020.08.005 |
| Citation | Julien A, et al. (2020) FGFR3 in Periosteal Cells Drives Cartilage-to-Bone Transformation in Bone Repair. Stem Cell Reports 15(4):955-967 |
| abstractText | Most organs and tissues in the body, including bone, can repair after an injury due to the activation of endogenous adult stem/progenitor cells to replace the damaged tissue. Inherent dysfunctions of the endogenous stem/progenitor cells in skeletal repair disorders are still poorly understood. Here, we report that Fgfr3(Y637C/+) over-activating mutation in Prx1-derived skeletal stem/progenitor cells leads to failure of fracture consolidation. We show that periosteal cells (PCs) carrying the Fgfr3(Y637C/+) mutation can engage in osteogenic and chondrogenic lineages, but following transplantation do not undergo terminal chondrocyte hypertrophy and transformation into bone causing pseudarthrosis. Instead, Prx1(Cre);Fgfr3(Y637C/+) PCs give rise to fibrocartilage and fibrosis. Conversely, wild-type PCs transplanted at the fracture site of Prx1(Cre);Fgfr3(Y637C/+) mice allow hypertrophic cartilage transition to bone and permit fracture consolidation. The results thus highlight cartilage-to-bone transformation as a necessary step for bone repair and FGFR3 signaling within PCs as a key regulator of this transformation. |
