|
| Cell types | Gli1+ cells [50, 51] | Axin2+ cells [46] | Postnatal Prx1+ cells [52] |
|
| Distribution | Early stage | All over the periosteum, dura, and the craniofacial sutures | In the calvarial sutures | In the calvarial sutures |
| One month after birth | Self-renewal | Only in the sutures | / |
| Stemness | Self-renewal | | Slow-cycling cells | |
| Contribution to other tissues | Suture mesenchyme, periosteum, dura mater, and parts of the calvarial bones | Suture mesenchyme and bone matrix near the osteogenic fronts | All calvarial tissues, except bone marrow osteoblasts |
| Ability to repair the defect | Unequivocal and potentially exclusive contribution of the sutural mesenchyme to calvarial injury repair |
| Ablation | Craniosynostosis | Craniosynostosis | Did not result in craniosynostosis or any other major craniofacial phenotype |
| MSC markers | CD90, CD73, CD44, Sca1, and CD146 | LepR | Pdgfrα and Mcam/CD146 (upregulation), Ccne2, Mcm4, and Pcna (downregulation), Itga2, Itga3, and Itga6 |
| Differentiation | Osteoblasts | + | +
(upon external stimulation) | +
(stimulated with recombinant WNT3A) |
| Chondrocytes | + | +
(upon external stimulation) | / |
| Adipocytes | + | / | / |
| Foundation of each study | Gli1 is the master transcriptional factor of hedgehog signaling and is indispensable for bone development and homeostasis. Gli1+ stem cells have been identified in canine and long bones. | Axin2 plays an irreplaceable role in the Wnt, BMP, and FGF signaling pathways; Axin2 knockout mice showed craniosynostosis. | Prx1 was previously shown to be highly expressed during limb bud formation and craniofacial development. |
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