The effects of tissue‐non‐specific alkaline phosphatase gene therapy on craniosynostosis and craniofacial morphology in the FGFR2C342Y/+ mouse model of Crouzon craniosynostosis
dc.contributor.author | Wang, E. | en_US |
dc.contributor.author | Nam, H. K. | en_US |
dc.contributor.author | Liu, J. | en_US |
dc.contributor.author | Hatch, N. E. | en_US |
dc.date.accessioned | 2015-05-04T20:36:53Z | |
dc.date.available | 2016-05-10T20:26:28Z | en |
dc.date.issued | 2015-04 | en_US |
dc.identifier.citation | Wang, E.; Nam, H. K.; Liu, J.; Hatch, N. E. (2015). "The effects of tissue‐non‐specific alkaline phosphatase gene therapy on craniosynostosis and craniofacial morphology in the FGFR2C342Y/+ mouse model of Crouzon craniosynostosis." Orthodontics & Craniofacial Research : 196-206. | en_US |
dc.identifier.issn | 1601-6335 | en_US |
dc.identifier.issn | 1601-6343 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/111219 | |
dc.publisher | Chapman & Hall/CRC | en_US |
dc.publisher | Wiley Periodicals, Inc. | en_US |
dc.subject.other | mouse model | en_US |
dc.subject.other | bone | en_US |
dc.subject.other | craniofacial | en_US |
dc.subject.other | craniosynostosis | en_US |
dc.subject.other | mineralization | en_US |
dc.title | The effects of tissue‐non‐specific alkaline phosphatase gene therapy on craniosynostosis and craniofacial morphology in the FGFR2C342Y/+ mouse model of Crouzon craniosynostosis | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Dentistry | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/111219/1/ocr12080.pdf | |
dc.identifier.doi | 10.1111/ocr.12080 | en_US |
dc.identifier.source | Orthodontics & Craniofacial Research | en_US |
dc.identifier.citedreference | Whyte MP. Physiological role of alkaline phosphatase explored in hypophosphatasia. Ann N Y Acad Sci 2010; 1192: 190 – 200. | en_US |
dc.identifier.citedreference | Johnson K, Moffa A, Chen Y, Pritzker K, Goding J, Terkeltaub R. Matrix vesicle plasma cell membrane glycoprotein‐1 regulates mineralization by murine osteoblastic MC3T3 cells. J Bone Miner Res 1999; 14: 883 – 92. | en_US |
dc.identifier.citedreference | Johnson KA, Hessle L, Vaingankar S, Wennberg C, Mauro S, Narisawa S et al. Osteoblast tissue‐nonspecific alkaline phosphatase antagonizes and regulates PC‐1. Am J Physiol Regul Integr Comp Physiol 2000; 279: R1365 – 77. | en_US |
dc.identifier.citedreference | Hessle L, Johnson KA, Anderson HC, Narisawa S, Sali A, Goding JW et al. Tissue‐nonspecific alkaline phosphatase and plasma cell membrane glycoprotein‐1 are central antagonistic regulators of bone mineralization. Proc Natl Acad Sci 2002; 99: 9445 – 9. | en_US |
dc.identifier.citedreference | Register TC, Wuthier RE. Effect of pyrophosphate and two diphosphonates on 45Ca and 32Pi uptake and mineralization by matrix vesicle‐enriched fractions and by hydroxyapatite. Bone 1985; 6: 307 – 12. | en_US |
dc.identifier.citedreference | Johnson K, Pritzker K, Goding J, Terkeltaub R. The nucleoside triphosphate pyrophosphohydrolase isozyme PC‐1 directly promotes cartilage calcification through chondrocyte apoptosis and increased calcium precipitation by mineralizing vesicles. J Rheumatol 2001; 8: 2681 – 91. | en_US |
dc.identifier.citedreference | Johnson K, Goding J, VanEtten D, Sali A, Hu S, Farley D et al. Linked deficiencies in extracellular PPi and osteopontin mediate pathologic calcification associated with defective PC‐1 and ANK expression. J Bone Min Res 2003; 1: 994 – 1004. | en_US |
dc.identifier.citedreference | Thouverey C, Bechkoff G, Pikula S, Buchet R. Inorganic pyrophosphate as a regulator of hydroxyapatite or calcium pyrophosphate dihydrate mineral deposition by matrix vesicles. Osteoarthritis Cartilage 2009; 17: 64 – 72. | en_US |
dc.identifier.citedreference | Beck GR Jr, Zerler B, Moran E. Phosphate is a specific signal for induction of osteopontin gene expression. Proc Natl Acad Sci USA 2000; 97: 8352 – 7. | en_US |
dc.identifier.citedreference | Polewski MD, Johnson KA, Foster M, Millán JL, Terkeltaub R. Inorganic pyrophosphatase induces type I collagen in osteoblasts. Bone 2010; 46: 81 – 90. | en_US |
dc.identifier.citedreference | Nam HK, Liu J, Li Y, Kragor A, Hatch NE. Ectonucleotide pyrophosphatase/phosphodiesterase‐1 (ENPP1) protein regulates osteoblast differentiation. J Biol Chem 2011; 286: 39059 – 71. | en_US |
dc.identifier.citedreference | Collmann H, Mornet E, Gattenlöhner S, Beck C, Girschick H. Neurosurgical aspects of childhood hypophosphatasia. Childs Nerv Syst 2009; 25: 217 – 23. | en_US |
dc.identifier.citedreference | Mornet E. Hypophosphatasia. Orphanet J Rare Dis 2007; 2: 40. | en_US |
dc.identifier.citedreference | Whyte MP, Greenberg CR, Salman NJ, Bober MB, McAlister WH, Wenkert D et al. Enzyme‐replacement therapy in life‐threatening hypophosphatasia. N Engl J Med 2012; 366: 904 – 13. | en_US |
dc.identifier.citedreference | Hatch NE, Nociti F, Swanson E, Bothwell M, Somerman M. FGF2 alters expression of the pyrophosphate/phosphate regulating proteins, PC‐1, ANK and TNAP, in the calvarial osteoblastic cell line, MC3T3E1(C4). Connect Tissue Res 2005; 46 ( 4–5 ): 184 – 92. | en_US |
dc.identifier.citedreference | Hatch NE, Li Y, Franceschi RT. FGF2 stimulation of the pyrophosphate‐generating enzyme, PC‐1, in pre‐osteoblast cells is mediated by RUNX2. J Bone Miner Res 2009; 24: 652 – 62. | en_US |
dc.identifier.citedreference | Yamamoto S, Orimo H, Matsumoto T, Iijima O, Narisawa S, Maeda T et al. Prolonged survival and phenotypic correction of Akp2(‐/‐) hypophosphatasia mice by lentiviral gene therapy. J Bone Miner Res 2011; 26: 135 – 42. | en_US |
dc.identifier.citedreference | Nishioka T, Tomatsu S, Gutierrez MA, Miyamoto K, Trandafirescu GG, Lopez PL et al. Enhancement of drug delivery to bone: characterization of human tissue‐nonspecific alkaline phosphatase tagged with an acidic oligopeptide. Mol Genet Metab 2006; 88: 244 – 55. | en_US |
dc.identifier.citedreference | Richtsmeier JT, Baxter LL, Reeves RH. Parallels of craniofacial maldevelopment in Down syndrome and Ts65Dn mice. Dev Dyn 2000; 217: 137 – 45. | en_US |
dc.identifier.citedreference | Lele S, Richtsmeier JT. An Invariant Approach to Statistical Analysis of Shapes. Boca Raton, FL: Chapman & Hall/CRC; 2001. | en_US |
dc.identifier.citedreference | Millan JL, Narisawa S, Lemire I, Loisel TP, Boileau G, Leonard P et al. Enzyme replacement therapy for murine hypophosphatasia. J Bone Miner Res 2008; 23: 777 – 87. | en_US |
dc.identifier.citedreference | Yadav MC, Lemire I, Leonard P, Boileau G, Blond L, Beliveau M et al. Dose response of bone‐targeted enzyme replacement for murine hypophosphatasia. Bone 2011; 49: 250 – 6. | en_US |
dc.identifier.citedreference | Rasmussen SA, Yazdy MM, Frías JL, Honein MA. Priorities for public health research on craniosynostosis: summary and recommendations from a Centers for Disease Control and Prevention‐sponsored meeting. Am J Med Genet A 2008; 146A: 149 – 58. | en_US |
dc.identifier.citedreference | Baird LC, Gonda D, Cohen SR, Evers LH, Lefloch N, Levy ML et al. Craniofacial reconstruction as a treatment for elevated intracranial pressure. Childs Nerv Syst 2011; 28: 411 – 18. | en_US |
dc.identifier.citedreference | Warren SM, Proctor MR, Bartlett SP, Blount JP, Buchman SR, Burnett W et al. Parameters of care for craniosynostosis: craniofacial and neurologic surgery perspectives. Plast Reconstr Surg 2012; 129: 731 – 7. | en_US |
dc.identifier.citedreference | Hatch NE. FGF signaling in craniofacial biological control and pathological craniofacial development. Crit Rev Eukaryot Gene Expr 2010; 20: 295 – 311. | en_US |
dc.identifier.citedreference | Eswarakumar VP, Horowitz MC, Locklin R, Morriss‐Kay GM, Lonai P. A gain‐of‐function mutation of Fgfr2c demonstrates the roles of this receptor variant in osteogenesis. Proc Natl Acad Sci USA 2004; 101: 12555 – 60. | en_US |
dc.identifier.citedreference | Perlyn CA, DeLeon VB, Babbs C, Govier D, Burell L, Darvann T et al. The craniofacial phenotype of the Crouzon mouse: analysis of a model for syndromic craniosynostosis using three‐dimensional MicroCT. Cleft Palate Craniofac J 2006; 43: 740. | en_US |
dc.identifier.citedreference | Liu J, Nam HK, Wang E, Hatch NE. Further analysis of the Crouzon mouse: effects of the FGFR2(C342Y) mutation are cranial bone‐dependent. Calcif Tissue Int 2013; 92: 451 – 66. | en_US |
dc.identifier.citedreference | Chen L, Li D, Li C, Engel A, Deng CX. A Ser252Trp [corrected] substitution in mouse fibroblast growth factor receptor 2 (Fgfr2) results in craniosynostosis. Bone 2003; 33: 169 – 78. | en_US |
dc.identifier.citedreference | Yin L, Du X, Li C, Xu X, Chen Z, Su N et al. A Pro253Arg mutation in fibroblast growth factor receptor 2 (Fgfr2) causes skeleton malformation mimicking human Apert syndrome by affecting both chondrogenesis and osteogenesis. Bone 2008; 42: 631 – 43. | en_US |
dc.identifier.citedreference | Twigg SR, Healy C, Babbs C, Sharpe JA, Wood WG, Sharpe PT et al. Skeletal analysis of the Fgfr 3(P244R) mouse, a genetic model for the Muenke craniosynostosis syndrome. Dev Dyn 2009; 238: 331 – 42. | en_US |
dc.identifier.citedreference | Murshed M, Harmery D, Millan JL, McKee MD, Karsenty G. Unique coexpression I osteoblasts of broadly expressed genes accounts for the spatial restriction of ECM mineralization to bone. Genes Dev 2009; 19: 1093 – 104. | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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