| First Author | Menon S | Year | 2021 |
| Journal | Nat Commun | Volume | 12 |
| Issue | 1 | Pages | 4640 |
| PubMed ID | 34330896 | Mgi Jnum | J:323034 |
| Mgi Id | MGI:6753891 | Doi | 10.1038/s41467-021-24801-6 |
| Citation | Menon S, et al. (2021) Skeletal stem and progenitor cells maintain cranial suture patency and prevent craniosynostosis. Nat Commun 12(1):4640 |
| abstractText | Cranial sutures are major growth centers for the calvarial vault, and their premature fusion leads to a pathologic condition called craniosynostosis. This study investigates whether skeletal stem/progenitor cells are resident in the cranial sutures. Prospective isolation by FACS identifies this population with a significant difference in spatio-temporal representation between fusing versus patent sutures. Transcriptomic analysis highlights a distinct signature in cells derived from the physiological closing PF suture, and scRNA sequencing identifies transcriptional heterogeneity among sutures. Wnt-signaling activation increases skeletal stem/progenitor cells in sutures, whereas its inhibition decreases. Crossing Axin2(LacZ/+) mouse, endowing enhanced Wnt activation, to a Twist1(+/-) mouse model of coronal craniosynostosis enriches skeletal stem/progenitor cells in sutures restoring patency. Co-transplantation of these cells with Wnt3a prevents resynostosis following suturectomy in Twist1(+/-) mice. Our study reveals that decrease and/or imbalance of skeletal stem/progenitor cells representation within sutures may underlie craniosynostosis. These findings have translational implications toward therapeutic approaches for craniosynostosis. |
