Expression of Runx2 and type X collagen in vertebral growth plate of patients with adolescent idiopathic scoliosis

Connective Tissue Research

Volumn 51, Issue 3, 2010, Pages 188-196

  Wang, Shoufeng ^a   Qiu, Yong ^a   Ma, Zhaolong ^a   Xia, Caiwei ^a   Zhu, Feng ^a   Zhu, Zezhang ^a  

^a MEDICAL SCHOOL OF NANJING UNIVERSITY   (China)

Author keywords

Condrocytes; Growth Plate; Idiopathic Scoliosis; Runx2; Type X Collagen

Indexed keywords

COLLAGEN TYPE 10; MESSENGER RNA; TRANSCRIPTION FACTOR RUNX2; RUNX2 PROTEIN, HUMAN;

ADOLESCENT; ADULT; ARTICLE; CARTILAGE CELL; CELL DENSITY; CHILD; CLINICAL ARTICLE; CONTROLLED STUDY; DISEASE COURSE; FEMALE; GROWTH PLATE; HISTOLOGY; HUMAN; HUMAN CELL; HUMAN TISSUE; IDIOPATHIC SCOLIOSIS; PROTEIN EXPRESSION; SCHOOL CHILD; VERTEBRA; ARTICULAR CARTILAGE; CHEMISTRY; ENZYME IMMUNOASSAY; GENE EXPRESSION; GENETICS; IN SITU HYBRIDIZATION; METABOLISM; PATHOLOGY; SCOLIOSIS; SPINE;

ADOLESCENT; CARTILAGE, ARTICULAR; CHILD; CHONDROCYTES; COLLAGEN TYPE X; CORE BINDING FACTOR ALPHA 1 SUBUNIT; FEMALE; GENE EXPRESSION; GROWTH PLATE; HUMANS; IMMUNOENZYME TECHNIQUES; IN SITU HYBRIDIZATION; RNA, MESSENGER; SCOLIOSIS; SPINE;

EID: 77954661802     PISSN: 03008207     EISSN: 16078438     Source Type: Journal    
DOI: 10.3109/03008200903215590     Document Type: Article

References (70)

1. Loncar-Dusek,M., Pecina, M., and Prebeg, Z. (1991). A longitudinal study of growth velocity and development of secondary gender characteristics versus onset of idiopathic scoliosis. Clin. Orthop., 270, 278-282.
2. Lonstein, J.E., and Carlson, J.M. (1984). The prediction of curve progression in untreated idiopathic scoliosis during growth. J. Bone Joint Surg. Am., 66, 1061-1071.
3. Little, D.G., Song, K.M., Katz, D., et al. (2000). Relationship of peak height velocity to other maturity indicators in idiopathic scoliosis in girls. J. Bone Joint Surg. Am., 82-A, 685-693.
4. Roaf, R. (1966). The basic anatomy of scoliosis. J. Bone Joint Surg. Br., 48, 786-792.
5. Stokes, I.A., and Laible, J.P. (1990). Three-dimensional osseo-ligamentous model of the thorax representing initiation of scoliosis by asymmetric growth. J. Biomech., 23, 589-595.
6. Millner, P.A., and Dickson, R.A. (1996). Idiopathic scoliosis: biomechanics and biology. Eur. Spine J., 5, 362-373.
7. Roaf, R. (1958). Rotation movements of the spine with special reference to scoliosis. J. Bone. Joint Surg. (Br.), 40, 312-332.
8. Villemure, I., Aubin, C.E., Dansereau, J., et al. (2002). Simulation of progressive deformities in adolescent idiopathic scoliosis using a biomechanical model integrating vertebral growth modulation. J. Biomech. Eng., 124, 784-790.
9. Parent, S., Labelle, H., Skalli, W., et al. (2004). Vertebral wedging characteristic changes in scoliotic spines. Spine, 29, E455-E462.
10. Hunziker, E.B. (1994). Mechanism of longitudinal bone growth and its regulation by growth plate chondrocytes. Microscopy Research and Technique, 28, 505-519.
11. Hunziker, E.B., and Schenk, R.K. (1989). Physiological mechanisms adopted by chondrocytes in regulating longitudinal bone growth in rats. J. Physiol., 414, 55-71.
12. Wilsman, N.J., Farnum, C.E., Leiferamn, E.M., et al. (1996). Differential growth by growth plates as a function of multiple parameters of chondrocytic kinetics. J. Orthop. Res., 14, 927-936.
13. Noonan, K.J., Hunziker, E.B., Nessler, J., and Buckwalter, J.A. (1998). Changes in cell, matrix compartment, and fibrillar collagen volumes between growth plate zones. J. Orthop. Res., 16, 500-580.
14. Hunziker, E.B., Schenk, P.K., and Cruz-Orive, L.M. (1987). Quantitation of chodrocyte performance in growth plate cartilage during longitudinal bone growth. J. Bone Joint Surg. (Am)., 69, 162-173.
15. Komori, T. (2002). Runx2, a multifunctional transcription factor in skeletal development. J. Cell Biochem., 87, 1-8.
16. Inada, M., Yasui, T., Nomura, S., et al. (1999). Maturational disturbance of chondrocytes in Cbfa1-deficient mice. Dev. Dyn., 214, 279-290.
17. Kim, I.S., Otto, F., Zabel, B., and Mundlos, S. (1999). Regulation of chondrocyte differentiation by Cbfa1. Mech. Dev., 80, 159-170.
18. Takeda, S., Bonnamy, J.P., Owen, M.J., et al. (2001). Continuous expression of Cbfa1 in nonhypertrophic chondrocytes uncovers its ability to induce hypertrophic chondrocyte differentiation and partially rescues Cbfa1-deficient mice. Genes Dev., 15, 467-481.
19. Ueta, C., Iwamoto, M., Kanatani, N., et al. (2001). Skeletal malformations caused by overexpression of Cbfa1 or its dominant negative form in chondrocytes. J. Cell Biol., 153, 87-100.
20. Ferguson, C., Alpern, E., Miclau, T., and Helms, J.A. (1999). Does adult fracture repair recapitulate embryonic skeletal formation? Mech. Dev., 87, 57-66.
21. Gao, Y.H., Shinki, T., Yuasa, T., et al. (1998). Potential role of cbfa1, an essential transcriptional factor for osteoblast differentiation, in osteoclastogenesis: regulation of mRNA expression of osteoclast differentiation factor ODF. Biochem. Biophys. Res. Commun., 252, 697-702.
22. Thirunavukkarasu, K., Halladay, D.L., Miles, R.R., et al. (2000). The osteoblast-specific transcription factor Cbfa1 contributes to the expression of osteoprotegerin, a potent inhibitor of osteoclast differentiation and function. J. Biol. Chem., 275, 25163-25172.
23. Zelzer, E., Glotzer, D.J., Hartmann, C., et al. (2001). Tissue specific regulation of VEGF expression during bone development requires Cbfa1/Runx2. Mech. Dev., 106, 97-106.
24. Zheng, Q., Zhou, G., Morello, R., et al. (2003). Type X collagen gene regulation by Runx2 contributes directly to its hypertrophic chondrocytespecific expression in vivo. J. Cell Biol., 162(5), 833-842.
25. Lenke, L.G., Betz, R.R., Harms, J., et al. (2001). Adolescent idiopathic scoliosis: a new classification to determine extent of spinal arthrodesis. J. Bone Joint Surg., 80, 1169-1181.
26. Rabie, A.B.M., Tang, G.H., and Urban, Hagg. (2004). Cbfa1 couples chondrocytes maturation and endochondral ossification in rat mandibular condylar cartilage. Arch. Oral Biol., 49, 109-118.
27. Chuma, A., Kitahara, H., Minami, S., Goto, S., Takaso, M., and Moriya, H. (1997). Structural scoliosis model in dogs with experimentally induced syringomyelia. Spine, 22, 589-594.
28. Deguchi, M., Kawakami, N., Kanemura, T., Mimatsu, K., and Iwata, H. (1995). Experimental scoliosis induced by rib resection in chicken. J. Spinal Disord., 8, 179-185.
29. Mente, P.L., Stokes, I.A., Spence, H., and Aronsson, D.D. (1997). Progression of vertebralwedging in an asymmetrically loaded rat tail model. Spine, 22, 1292-1296.
30. Hueter, C. (1862). Anatomische studien an den extremitaetengelenken neugeborener und erwachsener. Birkows Archiv. Path Anat. Physiol., 25, 572-599.
31. Bonnel, F., Dimeglio, A., Baldet, P., and Rabischong, P. (1984). Biomechanical activity of the growth plate. Clinical incidences. Anat. Clin., 6, 53-61.
32. Stokes, I.A.F., Aronsson, D.D., and Urban, J.P.G. (1994). Biomechanical factors influencing progression of angular skeletal deformities during growth. Eur. J. Musculoskel. Res., 3, 51-60.
33. Frost, H.M. (1990). Skeletal structural adaptations to mechanical usage (SATMU): 3. The hyaline cartilage modeling problem. Anat. Rec., 226, 423-432.
34. Leveau, BF, and Bernhardt, DB. (1984). Developmental biomechanics. Effect of forces on the growth, development, andmaintenance of the human body. Phys. Ther., 64, 1874-1882.
35. Bunnell, W.P. (1986). The natural history of idiopathic scoliosis before skeletal maturity. Spine, 11, 773-776.
36. Ylikoski,M. (1993). Spinal growth and progression of adolescent idiopathic scoliosis. Eur. Spine J., 1, 236-239.
37. Duval-Beaupere, G. (1971). Pathogenic relationship between scoliosis and growth. In Scoliosis and Growth, P.A. Zorab, (ed.). Edinburgh: Churchill Livingstone.
38. Ponseti, I.V., Pedrini, V., Wynne-Davies, R., et al. (1976). Pathogenesis of scoliosis. Clin. Orthop., 120, 268-280.
39. Bick, E.M., and Copel, J.W. (1950). Longitudinal growth of the human vertebra: a contribution to human osteogeny. J. Bone Joint Surg. [Amö., 32, 803-814.
40. Stilwell, D.L., Jr. (1962). Structural deformities of vertebrae. Bone adaptation and modeling in experimental scoliosis and kyphosis. Am. J. Orthop, 44, 611-634.
41. Michelsson, J.E. (1965). The development of spinal deformity in experimental scoliosis. Acta Orthop. Scand., 81(suppl), 1-91.
42. McCarroll, H.R., and Costen, W. (1960). Attempted treatment of scoliosis by unilateral vertebral epiphyseal arrest. J. Bone Joint Surg. (Am)., 42, 965-978.
43. Knutsson, F. (1963). A contribution to the discussion of the biological cause of idiopathic scoliosis. Acta Orthop. Scand., 33, 98-104.
44. Roaf, R. (1960). Vertebral growth and its mechanical control. J. Bone Joint Surg. Br., 42-B, 40-59.
45. Wang, S., Qiu, Y., Zhu, Z., et al. (2007). Histomorphological study of the spinal growth plates from the convex side and the concave side in adolescent idiopathic scoliosis. J. Orthop. Surg., 2, 19.
46. Aronsson, D.D., Stokes, I.A., Rosovsky, J., et al. (1999). Mechanical modulation of calf tail vertebral growth: implications for scoliosis progression. J. Spinal Disord., 12, 141-146.
47. Mente, P.L., Stokes, I.A., Spence, H., et al. (1997). Progression of vertebral wedging in an asymmetrically loaded rat tail model. Spine, 22, 1292-1296.
48. Mente, P.L., Aronsson, D.D., Stokes, I.A., et al. (1999). Mechanical modulation of growth for the correction of vertebral wedge deformities. J. Orthop. Res., 17, 518-524.
49. Nachlas, I.W., and Borden, J.N. (1950). Experimental scoliosis; the role of the epiphysis. Surg. Gynecol. Obstet., 90, 672-680.
50. Stokes, I.A., Spence, H., Aronsson, D.D., et al. (1996). Mechanical modulation of vertebral body growth. Implications for scoliosis progression. Spine, 21, 1162-1167.
51. Alvarez, J., Balbin,M., Santos, F., Fernandez, M., Ferrando, S., and Lopez, J.M. (2000). Different bone growth rates are associated with changes in the expression pattern of types II andXcollagens and collagenase 3 in proximal growth plates of the rat tibia. J. Bone Miner. Res., 15, 82-94.
52. Rabie, A.B., Shen, G., Hagg, U., et al. (2000). K Type X collagena marker for endochondral ossification of the mandibular condyles. Quintessence Orthodontics Yearbook (Japanese). Tokyo: Quintessence; p. 50-58.
53. Komori, T., and Kishimoto, T. (1998). Cbfa1 in bo
54. Enomoto, H., Enomoto-Iwamoto, M., Iwamoto, M., et al. (2000). Cbfa1 is a positive regulatory factor in chondrocyte maturation. J. Biol. Chem., 275, 8695-8702.
55. Harada, H., Tagashira, S., Fujiwara, M., et al. (1999). Cbfa1 isoforms exert functional differences in osteoblast differentiation. J. Biol. Chem., 274, 6972-6978.
56. Ducy, P., Zhang, R.,Geoffroy,V., et al. (1997).Osf2/Cbfa1: a transcriptional activator of osteoblast differentiation. Cell, 89, 747-754.
57. Lee, K.S., Kim, H.J., Li, Q.L., et al. (2000). Runx2 is a common target of transforming growth factor b1 and bone morphogeneticprotein 2, and cooperation between Runx2 and Smad5 induces osteoblast-specific gene expression in the pluripotent mesenchymalprecursor cell line C2C12. Mol. Cell Biol., 20, 8783-8792.
58. Kielty, C.M., Kwan, A.P.L., Holmes, D.F., et al. (1985). Type X collagen, a product of hypertrophic chondrocytes. Biochem. J., 227, 545-554.
59. Schmid, T.M., and Conrad, H.E. (1982). Metabolism of low molecular weight collagen by chondrocytes obtained from histologicallydistinct zones of the chick embryo tibiotarsus. J. Biol. Chem., 257, 12451-12457.
60. Haynes, J.S. (1990). Immunohistochemical localization of type X collagen in the proximal tibiotarsi of broiler chickens and turkeys. Anat. Rec., 227, 307-313.
61. Kirsch, T., and von der, Mark K. (1990). Isolation of bovine type X collagen and immunolocalization in growth-plate cartilage. Biochem. J., 265, 453-459.
62. Quarto, R., Dozin, B., Tacchetti, C., et al. (1990). In vitro development of hypertrophic chondrocytesstarting from selected clones of dedifferentiated cells. J. Cell Biol., 110, 1379-1386.
63. Schmid, T.M., Popp, R.G., and Linsenmayer, T.F. (1990). Hypertrophic cartilage matrix. Type X collagen, supramolecular assembly, and calcification. Ann. NY Acad. Sci., 580, 64-73.
64. Iyama, K., Ninomiya, Y., Olsen, B.R., et al. (1991). Spatiotemporal pattern of type X collagen gene expression and collagen deposition in embryonic chick vertebrae undergoing endochondral ossification. Anat. Rec., 29, 462-472
65. Alberty, A., Peltonen, J., and Ritsila, V. (1993). Effects of distraction and compression on proliferation of growth plate chondrocytes. A study in rabbits. Acta Orthop. Scand., 64, 449-455. (Pubitemid 23304187)
66. Ehrlich, M.G., Mankin, H.J., and Treadwell, B.V. (1972). Biochemical and physiological events during closure of the stapled distal femoral epiphyseal plate in rats. J. Bone Joint Surg. (Am)., 54, 309-322.
67. Bachrach, N.M. (1995). Growth plate chondrocyte deformation in situ and a biphasic inclusion model for cells within hydrated soft tissues. Ph.D. Thesis, Graduate School of Arts and Sciences, Columbia University, New York, NY, p. 254.
68. Farnum, C.E., Nixon, A., Lee, A.O., Kwan, D.T., Belanger, L., and Wilsman, N.J. (2000). Quantitative three-dimensional analysis of chondrocytic kinetic responses to short-term stapling of the rat proximal tibial growth plate. Cells Tissues Organs, 167, 247-258.
69. Stokes, I.A.F., Mente, P.L., latridis, J.C., Farnum, C.E., and Aronsson, D.D. (2002). Enlargement of growth plate chondrocytes modulated by sustained mechanical loading. J. Bone Joint Surg. (Am)., 84, 1842-1848.
70. Villemure, I., Chung, M.A., Seck, C.S., et al. (2005). Static compressive loading reduces the mRNA expression of type II and X collagen in rat growth-plate chondrocytes during postnatal growth. Connect. Tissue Res., 46, 211-219.