title: The suture provides a niche for mesenchymal stem cells of craniofacial bones.
abstract: Bone tissue undergoes constant turnover supported by stem cells. Recent studies showed that perivascular mesenchymal stem cells (MSCs) contribute to the turnover of long bones. Craniofacial bones are flat bones derived from a different embryonic origin than the long bones. The identity and regulating niche for craniofacial-bone MSCs remain unknown. Here, we identify Gli1+ cells within the suture mesenchyme as the main MSC population for craniofacial bones. They are not associated with vasculature, give rise to all craniofacial bones in the adult and are activated during injury repair. Gli1+ cells are typical MSCs in vitro. Ablation of Gli1+ cells leads to craniosynostosis and arrest of skull growth, indicating that these cells are an indispensable stem cell population. Twist1(+/-) mice with craniosynostosis show reduced Gli1+ MSCs in sutures, suggesting that craniosynostosis may result from diminished suture stem cells. Our study indicates that craniofacial sutures provide a unique niche for MSCs for craniofacial bone homeostasis and repair.
authors: Center for Craniofacial Molecular Biology, Ostrow School of Dentistry, University of Southern California, 2250 Alcazar Street, CSA 103 Los Angeles, California 90033, USA.
authors: Hu
authors: H
authors: Zhao
authors: Center for Craniofacial Molecular Biology, Ostrow School of Dentistry, University of Southern California, 2250 Alcazar Street, CSA 103 Los Angeles, California 90033, USA.
authors: Jifan
authors: J
authors: Feng
authors: Center for Craniofacial Molecular Biology, Ostrow School of Dentistry, University of Southern California, 2250 Alcazar Street, CSA 103 Los Angeles, California 90033, USA.
authors: Thach-Vu
authors: TV
authors: Ho
authors: Center for Craniofacial Molecular Biology, Ostrow School of Dentistry, University of Southern California, 2250 Alcazar Street, CSA 103 Los Angeles, California 90033, USA.
authors: Weston
authors: W
authors: Grimes
authors: Center for Craniofacial Molecular Biology, Ostrow School of Dentistry, University of Southern California, 2250 Alcazar Street, CSA 103 Los Angeles, California 90033, USA.
authors: Mark
authors: M
authors: Urata
authors: Center for Craniofacial Molecular Biology, Ostrow School of Dentistry, University of Southern California, 2250 Alcazar Street, CSA 103 Los Angeles, California 90033, USA.
authors: Yang
authors: Y
authors: Chai
mesh_terms: D000813:Anilides / Q000494:pharmacology; D000818:Animals; D002454:Cell Differentiation / Q000235:genetics; D003393:Cranial Sutures / Q000098:blood supply / Q000166:cytology* / Q000254:growth & development; D003398:Craniosynostoses / Q000235:genetics*; D017102:Fracture Healing / Q000235:genetics; D053823:Hedgehog Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism; D051741:Kruppel-Like Transcription Factors / Q000235:genetics* / Q000378:metabolism; D059630:Mesenchymal Stem Cells / Q000166:cytology*; D051379:Mice; D008822:Mice, Transgenic; D009687:Nuclear Proteins / Q000235:genetics*; D010024:Osteoporosis / Q000235:genetics; D011725:Pyridines / Q000494:pharmacology; D043562:Receptors, G-Protein-Coupled / Q000235:genetics; D000072086:Smoothened Receptor; D051879:Twist-Related Protein 1 / Q000235:genetics*; D000071676:Zinc Finger Protein GLI1
chemical_list: D000813:Anilides; C498520:Gli1 protein, mouse; D053823:Hedgehog Proteins; C538724:HhAntag691; D051741:Kruppel-Like Transcription Factors; D009687:Nuclear Proteins; D011725:Pyridines; D043562:Receptors, G-Protein-Coupled; C465570:Shh protein, mouse; C491022:Smo protein, mouse; D000072086:Smoothened Receptor; D051879:Twist-Related Protein 1; D000071676:Zinc Finger Protein GLI1; C514061:ihh protein, mouse; C067250:Twist1 protein, mouse