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Selected Publications 

1.      Skeletal stem and progenitor cells maintain cranial suture patency and prevent craniosynostosis. Menon S, Salhotra A, Shailendra S, Tevlin R, Ransom RC, Januszyk M, Chan CKF, Behr B, Wan DC, Longaker MT, Quarto N. Nat Commun. 2021 Jul 30;12(1):4640

2.      Harnessing a Feasible and Versatile ex vivo Calvarial Suture 2-D Culture System to Study Suture Biology.  Quarto N, Menon S, Griffin M, Huber J, Longaker MT. Front Physiol. 2022 Feb 10;13:823661. doi: 10.3389/fphys.2022.823661. eCollection 2022.

3.      Absence of endochondral ossification and craniosynostosis in posterior frontal cranial sutures of Axin2(-/-) mice.  Behr B, Longaker MT, Quarto N. PLoS One. 2013 Aug 1;8(8):e70240. doi: 10.1371/journal.pone.0070240.

4.      Differential activation of canonical Wnt signaling determines cranial sutures fate: a novel mechanism for sagittal suture craniosynostosis.  Behr B, Longaker MT, Quarto N. Dev Biol. 2010 Aug 15;344(2):922-40. doi: 10.1016/j.ydbio.2010.06.009.

5.      Sox9 neural crest determinant gene controls patterning and closure of the posterior frontal cranial suture.  Sahar DE, Longaker MT, Quarto N. Dev Biol. 2005 Apr 15;280(2):344-61. doi: 10.1016/j.ydbio.2005.01.022.60

6.      Craniosynostosis of coronal suture in twist1 mice occurs through endochondral ossification recapitulating the physiological closure of posterior frontal suture.  Behr B, Longaker MT, Quarto N. Front Physiol. 2011 Jul 21;2:37. doi: 10.3389/fphys.2011.00037.

1.     Menon S, Huber J, Duldulao C, Longaker MT, Quarto N. An Evolutionary Conserved Signaling Network Between Mouse and Human Underlies the Differential Osteoskeletal Potential of Frontal and Parietal Calvarial Bones. Front Physiol. 2021 Oct 21;12:747091. doi: 10.3389/fphys.2021.747091. PMID: 34744787; PMCID: PMC8567095.

2.     Li S, Meyer NP, Quarto N, Longaker MT. Integration of multiple signaling regulates through apoptosis the differential osteogenic potential of neural crest-derived and mesoderm-derived Osteoblasts. Plos One. 2013;8(3):e58610. doi: 10.1371/journal.pone.0058610. PubMed PMID: 23536803; PubMed Central PMCID: PMC3607600.

3.     Quarto N, Wan DC, Kwan MD, Panetta NJ Origin matters: differences in embryonic tissue origin and Wnt signaling determine the osteogenic potential and healing capacity of frontal and parietal calvarial bones. J Bone Miner Res. 2010; 25 (7): 1680-94.

4.     Behr B, Panetta NJ, Longaker MT, Quarto N. Different endogenous threshold levels of Fibroblast Growth Factor-ligands determine the healing potential of frontal and parietal bones. Bone. 2010; 47 (2): 281-94.

5.     Li S, Quarto N, Longaker MT. Activation of FGF signaling mediates proliferative and osteogenic differences between neural crest derived frontal and mesoderm parietal derived bone. PLoS One. 2010; 5(11): e14033.

Selected Publications 

1.     Menon S, Huber J, Duldulao C, Longaker MT, Quarto N. An Evolutionary Conserved Signaling Network Between Mouse and Human Underlies the Differential Osteoskeletal Potential of Frontal and Parietal Calvarial Bones. Front Physiol. 2021 Oct 21;12:747091. doi: 10.3389/fphys.2021.747091. PMID: 34744787; PMCID: PMC8567095.

2.     Li S, Meyer NP, Quarto N, Longaker MT. Integration of multiple signaling regulates through apoptosis the differential osteogenic potential of neural crest-derived and mesoderm-derived Osteoblasts. Plos One. 2013;8(3):e58610. doi: 10.1371/journal.pone.0058610. PubMed PMID: 23536803; PubMed Central PMCID: PMC3607600.

3.     Quarto N, Wan DC, Kwan MD, Panetta NJ Origin matters: differences in embryonic tissue origin and Wnt signaling determine the osteogenic potential and healing capacity of frontal and parietal calvarial bones. J Bone Miner Res. 2010; 25 (7): 1680-94.

4.     Behr B, Panetta NJ, Longaker MT, Quarto N. Different endogenous threshold levels of Fibroblast Growth Factor-ligands determine the healing potential of frontal and parietal bones. Bone. 2010; 47 (2): 281-94.

5.     Li S, Quarto N, Longaker MT. Activation of FGF signaling mediates proliferative and osteogenic differences between neural crest derived frontal and mesoderm parietal derived bone. PLoS One. 2010; 5(11): e14033.

The craniofacial team at the Longaker lab focuses on two main areas:

Several papers have been published; describing the bio-molecular mechanism(s) governing the higher osteogenic potential and skeletal repair of the neural crest-derived frontal bone and its relationship to FGF, Wnt, and BMP signaling pathways.

Craniofacial Repair and Suture Biology 

1.     The first area of research is the developmental biology of cranial sutures, specifically, the posterior frontal (PF) suture (metopic in humans), which is a fusing suture, and the non-closing sagittal (Sag) and coronal (Cor) sutures. We have identified the timing and process through which the PF suture closes, showing that this suture fuses through an “autonomous” endochondral ossification process between embryonic days 14-17. Furthermore, we have identified canonical Wnt signaling as a major player in controlling the patency of cranial sutures. Our research extends also to pathological conditions such as craniosynostosis, a premature closure of cranial sutures.

Current studies are aimed towards establishing the presence of and characterization of stem cell population(s), to profile their molecular signature, and to determine how these stem cells may contribute to the different patterning/fate of the cranial sutures.

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2.     The second area of research is the developmental biology of cranial sutures, specifically, the posterior frontal (PF) suture (metopic in humans), which is a fusing suture, and the non-closing sagittal (Sag) and coronal (Cor) sutures. We have identified the timing and process through which the PF suture closes, showing that this suture fuses through an “autonomous” endochondral ossification process between embryonic days 14-17. Furthermore, we have identified canonical Wnt signaling as a major player in controlling the patency of cranial sutures. Our research extends also to pathological conditions such as craniosynostosis, a premature closure of cranial sutures.

Current studies are aimed towards establishing the presence of and characterization of stem cell population(s), to profile their molecular signature, and to determine how these stem cells may contribute to the different patterning/fate of the cranial sutures.

6f25d7_1b17f2473cc747c7bc399418a2a33a2c.webp

2.     The second area of investigation focuses on calvarial bones of different embryonic tissue origin and how these different tissue origins impact the osteogenic potential and skeletal repair of these bones. The current research focuses on the neural crest-derived frontal bone and paraxial mesoderm-derived parietal bone. This research has unveiled significant and substantial differences between frontal and parietal bones highlighting some of the molecular mechanism(s) responsible for the different osteogenic capacity and tissue repair potential observed between the two bones. The results gained from this investigation represent an important potential for translational implications to skeletal repair/regeneration.

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Moreover, our research spans also on pathological conditions determined by a misrepresentation of SSCs in the context of craniofacial development. Our recent findings have unveiled the importance of a proper balance of SSCs in their niche for the maintenance of cranial sutures patency. Our studies on animal models of craniosynostosis have shown a decrease representation of SSCs correlation to a suture fusion, conversely an increased representation correlates  to sustained suture patency.

Craniofacial Repair and Suture Biology 

The craniofacial team at the Longaker lab focuses on two main areas:

1.     The first area of research is the developmental biology of cranial sutures, specifically, the posterior frontal (PF) suture (metopic in humans), which is a fusing suture, and the non-closing sagittal (Sag) and coronal (Cor) sutures. We have identified the timing and process through which the PF suture closes, showing that this suture fuses through an “autonomous” endochondral ossification process between embryonic days 14-17. Furthermore, we have identified canonical Wnt signaling as a major player in controlling the patency of cranial sutures. Our research extends also to pathological conditions such as craniosynostosis, a premature closure of cranial sutures.

Current studies are aimed towards establishing the presence of and characterization of stem cell population(s), to profile their molecular signature, and to determine how these stem cells may contribute to the different patterning/fate of the cranial sutures.

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