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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 張雅珮 | |
| dc.contributor.author | Yen-Wen Liu | en |
| dc.contributor.author | 劉晏文 | zh_TW |
| dc.date.accessioned | 2021-06-17T04:57:06Z | - |
| dc.date.available | 2018-08-01 | |
| dc.date.copyright | 2018-08-01 | |
| dc.date.issued | 2018 | |
| dc.date.submitted | 2018-07-27 | |
| dc.identifier.citation | 邱柏喻. (2013). 硫酸乙醯肝素酶對小鼠骨癒合之影響. (碩士), 國立臺灣大學, 台 北市.
Åbrink, M., Grujic, M., & Pejler, G. (2004). Serglycin Is Essential for Maturation of Mast Cell Secretory Granule. Journal of Biological Chemistry, 279(39), 40897-40905. doi:10.1074/jbc.M405856200 Ai-Aql, Z. S., Alagl, A. S., Graves, D. T., Gerstenfeld, L. C., & Einhorn, T. A. (2008). Molecular Mechanisms Controlling Bone Formation during Fracture Healing and Distraction Osteogenesis. Journal of dental research, 87(2), 107-118. Akiyama, H., Chaboissier, M.-C., Martin, J. F., Schedl, A., & de Crombrugghe, B. (2002). The transcription factor Sox9 has essential roles in successive steps of the chondrocyte differentiation pathway and is required for expression of Sox5 and Sox6. Genes & Development, 16(21), 2813-2828. doi:10.1101/gad.1017802 Alatalo, S. L., Ivaska, K. K., Waguespack, S. G., Econs, M. J., Väänänen, H. K., & Halleen, J. M. (2004). Osteoclast-Derived Serum Tartrate-Resistant Acid Phosphatase 5b in Albers-Schönberg Disease (Type II Autosomal Dominant Osteopetrosis). Clinical Chemistry, 50(5), 883. Alexopoulou, A. N., Multhaupt, H. A. B., & Couchman, J. R. (2007). Syndecans in wound healing, inflammation and vascular biology. The International Journal of Biochemistry & Cell Biology, 39(3), 505-528. doi:https://doi.org/10.1016/j.biocel.2006.10.014 Bais, M., McLean, J., Sebastiani, P., Young, M., Wigner, N., Smith, T., . . . Gerstenfeld, L. C. (2009). Transcriptional Analysis of Fracture Healing and the Induction of Embryonic Stem Cell–Related Genes. PLOS ONE, 4(5), e5393. doi:10.1371/journal.pone.0005393 Bais, M. V., Wigner, N., Young, M., Toholka, R., Graves, D. T., Morgan, E. F., . . . Einhorn, T. A. (2009). BMP2 Is Essential for Post Natal Osteogenesis but Not for Recruitment of Osteogenic Stem Cells. Bone, 45(2), 254-266. doi:10.1016/j.bone.2009.04.239 Bandyopadhyay, A., Tsuji, K., Cox, K., Harfe, B. D., Rosen, V., & Tabin, C. J. (2006). Genetic Analysis of the Roles of BMP2, BMP4, and BMP7 in Limb Patterning and Skeletogenesis. PLoS Genetics, 2(12), e216. doi:10.1371/journal.pgen.0020216 Barna, M., & Niswander, L. (2007). Visualization of Cartilage Formation: Insight into Cellular Properties of Skeletal Progenitors and Chondrodysplasia Syndromes. Developmental Cell, 12(6), 931-941. doi:https://doi.org/10.1016/j.devcel.2007.04.016 Barnes, G. L., Kostenuik, P. J., Gerstenfeld, L. C., & Einhorn, T. A. (1999). Growth Factor Regulation of Fracture Repair. Journal of Bone and Mineral Research, 14(11), 1805-1815. doi:doi:10.1359/jbmr.1999.14.11.1805 Bigham-Sadegh, A., & Oryan, A. (2015). Basic concepts regarding fracture healing and the current options and future directions in managing bone fractures. International Wound Journal, 12(3), 238-247. doi:doi:10.1111/iwj.12231 Breur, G. J., Vanenkevort, B. A., Farnum, C. E., & Wilsman, N. J. (1991). Linear relationship between the volume of hypertrophic chondrocytes and the rate of longitudinal bone growth in growth plates. Journal of Orthopaedic Research, 9(3), 348-359. doi:doi:10.1002/jor.1100090306 Brown, A. J., Alicknavitch, M., D’Souza, S. S., Daikoku, T., Kirn-Safran, C. B., Marchetti, D., . . . Farach-Carson, M. C. (2008). Heparanase expression and activity influences chondrogenic and osteogenic processes during endochondral bone formation. Bone, 43(4), 689-699. doi:https://doi.org/10.1016/j.bone.2008.05.022 Caplan, A. I. (1987). Bone development and repair. BioEssays, 6(4), 171-175. doi:10.1002/bies.950060406 Carano, R. A. D., & Filvaroff, E. H. (2003). Angiogenesis and bone repair. Drug Discovery Today, 8(21), 980-989. doi:https://doi.org/10.1016/S1359-6446(03)02866-6 Charles, P., Hasling, C., Risteli, L., Risteli, J., Mosekilde, L., & Eriksen, E. F. (1992). Assessment of bone formation by biochemical markers in metabolic bone disease: Separation between osteoblastic activity at the cell and tissue level. Calcified Tissue International, 51(6), 406-411. doi:10.1007/bf00296671 Chen, C.-J., Chao, T.-Y., Chu, D.-M., Janckila, A. J., & Cheng, S.-N. (2004). Osteoblast and Osteoclast Activity in a Malignant Infantile Osteopetrosis Patient Following Bone Marrow Transplantation. Journal of Pediatric Hematology/Oncology, 26(1), 5-8. Chung, U.-i., Schipani, E., McMahon, A. P., & Kronenberg, H. M. (2001). Indian hedgehog couples chondrogenesis to osteogenesis in endochondral bone development. The Journal of Clinical Investigation, 107(3), 295-304. doi:10.1172/JCI11706 Desai, U. R., Wang, H. M., & Linhardt, R. J. (1993). Substrate Specificity of the Heparin Lyases from Flavobacterium heparinum. Archives of Biochemistry and Biophysics, 306(2), 461-468. doi:https://doi.org/10.1006/abbi.1993.1538 Dimitriou, R., Jones, E., McGonagle, D., & Giannoudis, P. V. (2011). Bone regeneration: current concepts and future directions. BMC Medicine, 9(1), 66. doi:10.1186/1741-7015-9-66 Dimitriou, R., Tsiridis, E., & Giannoudis, P. V. Current concepts of molecular aspects of bone healing. Injury, 36(12), 1392-1404. doi:10.1016/j.injury.2005.07.019 Dong, Y., Jesse, A. M., Kohn, A., Gunnell, L. M., Honjo, T., Zuscik, M. J., . . . Hilton, M. J. (2010). RBPj κ -dependent Notch signaling regulates mesenchymal progenitor cell proliferation and differentiation during skeletal development. Development (Cambridge, England), 137(9), 1461-1471. doi:10.1242/dev.042911 Du, X., Xie, Y., Xian, C. J., & Chen, L. (2012). Role of FGFs/FGFRs in skeletal development and bone regeneration. Journal of Cellular Physiology, 227(12), 3731-3743. doi:10.1002/jcp.24083 Einhorn, T. A. (1998). The cell and molecular biology of fracture healing. Clin Orthop Relat Res(355 Suppl), S7-21. Einhorn, T. A. (1998). The Cell and Molecular Biology of Fracture Healing. Clinical Orthopaedics and Related Research, 355, S7-S21. Eswarakumar, V. P., & Schlessinger, J. (2007). Skeletal overgrowth is mediated by deficiency in a specific isoform of fibroblast growth factor receptor 3. Proceedings of the National Academy of Sciences, 104(10), 3937-3942. doi:10.1073/pnas.0700012104 Fuster, M. M., & Esko, J. D. (2005). The sweet and sour of cancer: glycans as novel therapeutic targets. Nature Reviews Cancer, 5, 526. doi:10.1038/nrc1649 Gardnera, T. N., Stoll, T., Marks, L., Mishra, S., & Knothe Tate, M. The influence ofmechanical stimulus on the pattern of tissue differentiation in a long bone fracture — an FEM study. Journal of Biomechanics, 33(4), 415-425. doi:10.1016/S0021-9290(99)00189-X Gautam, M., DeChiara, T. M., Glass, D. J., Yancopoulos, G. D., & Sanes, J. R. (1999). Distinct phenotypes of mutant mice lacking agrin, MuSK, or rapsyn. Developmental Brain Research, 114(2), 171-178. doi:https://doi.org/10.1016/S0165-3806(99)00013-9 Gautam, M., Noakes, P. G., Moscoso, L., Rupp, F., Scheller, R. H., Merlie, J. P., & Sanes, J. R. Defective Neuromuscular Synaptogenesis in Agrin-Deficient Mutant Mice. Cell, 85(4), 525-535. doi:10.1016/S0092-8674(00)81253-2 Gerstenfeld, L. C., Alkhiary, Y. M., Krall, E. A., Nicholls, F. H., Stapleton, S. N., Fitch, J. L., . . . Einhorn, T. A. (2006). Three-dimensional Reconstruction of Fracture Callus Morphogenesis. Journal of Histochemistry & Cytochemistry, 54(11), 1215-1228. doi:10.1369/jhc.6A6959.2006 Gerstenfeld, L. C., Cullinane, D. M., Barnes, G. L., Graves, D. T., & Einhorn, T. A. (2003). Fracture healing as a post-natal developmental process: Molecular, spatial, and temporal aspects of its regulation. Journal of Cellular Biochemistry, 88(5), 873-884. doi:doi:10.1002/jcb.10435 Granero-Moltó, F., Weis, J. A., Miga, M. I., Landis, B., Myers, T. J., O’Rear, L., . . . Spagnoli, A. (2009). Regenerative Effects of Transplanted Mesenchymal Stem Cells in Fracture Healing. Stem cells (Dayton, Ohio), 27(8), 1887-1898. doi:10.1002/stem.103 Hill, T. P., Später, D., Taketo, M. M., Birchmeier, W., & Hartmann, C. (2005). Canonical Wnt/β-Catenin Signaling Prevents Osteoblasts from Differentiating into Chondrocytes. Developmental Cell, 8(5), 727-738. doi:https://doi.org/10.1016/j.devcel.2005.02.013 Hilton, M. J., Tu, X., Wu, X., Bai, S., Zhao, H., Kobayashi, T., . . . Long, F. (2008). Notch signaling maintains bone marrow mesenchymal progenitors by suppressing osteoblast differentiation. Nature medicine, 14(3), 306-314. doi:10.1038/nm1716 Holness, C. L., & Simmons, D. L. (1993). Molecular cloning of CD68, a human macrophage marker related to lysosomal glycoproteins. Blood, 81(6), 1607. Hu, H., Hilton, M. J., Tu, X., Yu, K., Ornitz, D. M., & Long, F. (2005). Sequential roles of Hedgehog and Wnt signaling in osteoblast development. Development, 132(1), 49. Hume, D. A. (2011). Applications of myeloid-specific promoters in transgenic mice support in vivo imaging and functional genomics but do not support the concept of distinct macrophage and dendritic cell lineages or roles in immunity. Journal of Leukocyte Biology, 89(4), 525-538. doi:doi:10.1189/jlb.0810472 Iozzo, R. V. (2005). Basement membrane proteoglycans: from cellar to ceiling. Nature Reviews Molecular Cell Biology, 6, 646. doi:10.1038/nrm1702 https://www.nature.com/articles/nrm1702 - supplementary-information Itoh, N., & Ornitz, D. M. (2008). Functional evolutionary history of the mouse Fgf gene family. Developmental Dynamics, 237(1), 18-27. doi:10.1002/dvdy.21388 Jackson, M. F., Scatena, M., & Giachelli, C. M. (2017). Osteoclast precursors do not express CD68: results from CD68 promoter-driven RANK transgenic mice. FEBS Letters, 591(5), 728-736. doi:doi:10.1002/1873-3468.12588 Jacob, A. L., Smith, C., Partanen, J., & Ornitz, D. M. (2006). Fibroblast growth factorreceptor 1 signaling in the osteo-chondrogenic cell lineage regulates sequential steps of osteoblast maturation. Developmental Biology, 296(2), 315-328. doi:https://doi.org/10.1016/j.ydbio.2006.05.031 Joeng, K. S., & Long, F. (2009). The Gli2 transcriptional activator is a crucial effector for Ihh signaling in osteoblast development and cartilage vascularization. Development (Cambridge, England), 136(24), 4177-4185. doi:10.1242/dev.041624 Kanwar, Y. S., Linker, A., & Farquhar, M. G. (1980). Increased permeability of the glomerular basement membrane to ferritin after removal of glycosaminoglycans (heparan sulfate) by enzyme digestion. The Journal of Cell Biology, 86(2), 688. Karaplis, A. C., Luz, A., Glowacki, J., Bronson, R. T., Tybulewicz, V. L., Kronenberg, H. M., & Mulligan, R. C. (1994). Lethal skeletal dysplasia from targeted disruption of the parathyroid hormone-related peptide gene. Genes & Development, 8(3), 277-289. doi:10.1101/gad.8.3.277 Karp, S. J., Schipani, E., St-Jacques, B., Hunzelman, J., Kronenberg, H., & McMahon, A. P. (2000). Indian hedgehog coordinates endochondral bone growth and morphogenesis via parathyroid hormone related-protein-dependent and -independent pathways. Development, 127(3), 543. Keramaris, N. C., Calori, G. M., Nikolaou, V. S., Schemitsch, E. H., & Giannoudis, P. V. (2008). Fracture vascularity and bone healing: a systematic review of the role of VEGF. Injury, 39 Suppl 2, S45-57. doi:10.1016/S0020-1383(08)70015-9 Ketenjian, A. Y., & Arsenis, C. (1975). Morphological and biochemical studies during differentiation and calcification of fracture callus cartilage. Clin Orthop Relat Res(107), 266-273. Kohn, A., Dong, Y., Mirando, A. J., Jesse, A. M., Honjo, T., Zuscik, M. J., . . . Hilton, M. J. (2012). Cartilage-specific RBPjκ-dependent and -independent Notch signals regulate cartilage and bone development. Development, 139(6), 1198. Kokabu, S., Gamer, L., Cox, K., Lowery, J., Tsuji, K., Raz, R., . . . Rosen, V. (2012). BMP3 Suppresses Osteoblast Differentiation of Bone Marrow Stromal Cells via Interaction with Acvr2b. Molecular Endocrinology, 26(1), 87-94. doi:10.1210/me.2011-1168 Komori, T., Yagi, H., Nomura, S., Yamaguchi, A., Sasaki, K., Deguchi, K., . . . Kishimoto, T. (1997). Targeted Disruption of Cbfa1 Results in a Complete Lack of Bone Formation owing to Maturational Arrest of Osteoblasts. Cell, 89(5), 755-764. doi:https://doi.org/10.1016/S0092-8674(00)80258-5 Kram, V., Zcharia, E., Yacoby-Zeevi, O., Metzger, S., Chajek-Shaul, T., Gabet, Y., . . . Bab, I. (2006). Heparanase is expressed in osteoblastic cells and stimulates bone formation and bone mass. Journal of Cellular Physiology, 207(3), 784-792. doi:10.1002/jcp.20625 Kronenberg, H. M. (2003). Developmental regulation of the growth plate. Nature, 423, 332. doi:10.1038/nature01657 Lanske, B., Karaplis, A. C., Lee, K., Luz, A., Vortkamp, A., Pirro, A., . . . Kronenberg, H. M. (1996). PTH/PTHrP Receptor in Early Development and Indian Hedgehog--Regulated Bone Growth. Science, 273(5275), 663. Lee, S.-K., & Lorenzo, J. (2006). Cytokines regulating osteoclast formation and function. Current Opinion in Rheumatology, 18(4), 411-418. doi:10.1097/01.bor.0000231911.42666.78 Lehmann, W., Edgar, C. M., Wang, K., Cho, T. J., Barnes, G. L., Kakar, S., . . . Einhorn, T. A. (2005). Tumor necrosis factor alpha (TNF-α) coordinatelyregulates the expression of specific matrix metalloproteinases (MMPS) and angiogenic factors during fracture healing. Bone, 36(2), 300-310. doi:10.1016/j.bone.2004.10.010 Li, J.-P., Galvis, M. L. E., Gong, F., Zhang, X., Zcharia, E., Metzger, S., . . . Lindahl, U. (2005). <em>In vivo</em> fragmentation of heparan sulfate by heparanase overexpression renders mice resistant to amyloid protein A amyloidosis. Proceedings of the National Academy of Sciences of the United States of America, 102(18), 6473. Lindahl, U., Kusche-Gullberg, M., & Kjellén, L. (1998). Regulated Diversity of Heparan Sulfate. Journal of Biological Chemistry, 273(39), 24979-24982. doi:10.1074/jbc.273.39.24979 Linhardt, R. J., Turnbull, J. E., Wang, H. M., Loganathan, D., & Gallagher, J. T. (1990). Examination of the substrate specificity of heparin and heparan sulfate lyases. Biochemistry, 29(10), 2611-2617. doi:10.1021/bi00462a026 Liu, Z., Lavine, K. J., Hung, I. H., & Ornitz, D. M. (2007). FGF18 is required for early chondrocyte proliferation, hypertrophy and vascular invasion of the growth plate. Developmental Biology, 302(1), 80-91. doi:https://doi.org/10.1016/j.ydbio.2006.08.071 Long, F., Chung, U.-i., Ohba, S., McMahon, J., Kronenberg, H. M., & McMahon, A. P. (2004). Ihh signaling is directly required for the osteoblast lineage in the endochondral skeleton. Development, 131(6), 1309. Long, F., Zhang, X. M., Karp, S., Yang, Y., & McMahon, A. P. (2001). Genetic manipulation of hedgehog signaling in the endochondral skeleton reveals a direct role in the regulation of chondrocyte proliferation. Development, 128(24), 5099. Lyon, M., & Gallagher, J. T. (1998). Bio-specific sequences and domains in heparan sulphate and the regulation of cell growth and adhesion. Matrix Biology, 17(7), 485-493. doi:https://doi.org/10.1016/S0945-053X(98)90096-8 Mansouri, R., Jouan, Y., Hay, E., Blin-Wakkach, C., Frain, M., Ostertag, A., . . . Modrowski, D. (2017). Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells. Cell Death & Disease, 8(6), e2902. doi:10.1038/cddis.2017.287 Mead, T. J., & Yutzey, K. E. (2009). Notch pathway regulation of chondrocyte differentiation and proliferation during appendicular and axial skeleton development. Proceedings of the National Academy of Sciences of the United States of America, 106(34), 14420-14425. doi:10.1073/pnas.0902306106 Minkin, C. (1982). Bone acid phosphatase: Tartrate-resistant acid phosphatase as a marker of osteoclast function. Calcified Tissue International, 34(1), 285-290. doi:10.1007/bf02411252 Monfoulet, L., Rabier, B., Chassande, O., & Fricain, J.-C. (2010). Drilled Hole Defects in Mouse Femur as Models of Intramembranous Cortical and Cancellous Bone Regeneration. Calcified Tissue International, 86(1), 72-81. doi:10.1007/s00223-009-9314-y Morgan, E. F., Giacomo, A., & Gerstenfeld, L. C. (2014). Overview of Skeletal Repair (Fracture Healing and Its Assessment) # T Skeletal Development and Repair (Vol. 1130, pp. 13-31). Murali, S., Rai, B., Dombrowski, C., Lee, J. L. J., Lim, Z. X. H., Bramono, D. S., . . . Cool, S. M. (2013). Affinity-selected heparan sulfate for bone repair.Biomaterials, 34(22), 5594-5605. doi:https://doi.org/10.1016/j.biomaterials.2013.04.017 Nakashima, K., Zhou, X., Kunkel, G., Zhang, Z., Deng, J. M., Behringer, R. R., & de Crombrugghe, B. (2002). The Novel Zinc Finger-Containing Transcription Factor Osterix Is Required for Osteoblast Differentiation and Bone Formation. Cell, 108(1), 17-29. doi:https://doi.org/10.1016/S0092-8674(01)00622-5 Naski, M. C., Colvin, J. S., Coffin, J. D., & Ornitz, D. M. (1998). Repression of hedgehog signaling and BMP4 expression in growth plate cartilage by fibroblast growth factor receptor 3. Development, 125(24), 4977. Ornitz, D. M., & Marie, P. J. (2002). FGF signaling pathways in endochondral and intramembranous bone development and human genetic disease. Genes & Development, 16(12), 1446-1465. doi:10.1101/gad.990702 Papy-Garcia, D., & Albanese, P. (2017). Heparan sulfate proteoglycans as key regulators of the mesenchymal niche of hematopoietic stem cells. Glycoconjugate Journal, 34(3), 377-391. doi:10.1007/s10719-017-9773-8 Parish, C. R. (2006). The role of heparan sulphate in inflammation. Nature Reviews Immunology, 6, 633. doi:10.1038/nri1918 Peterson, S. B., & Liu, J. (2013). Multi-faceted substrate specificity of heparanase. Matrix Biology, 32(5), 223-227. doi:https://doi.org/10.1016/j.matbio.2013.02.006 Pogue, R., & Lyons, K. (2006). BMP Signaling in the Cartilage Growth Plate Current Topics in Developmental Biology (Vol. 76, pp. 1-48): Academic Press. Roberts, S. J., van Gastel, N., Carmeliet, G., & Luyten, F. P. Uncovering the periosteum for skeletal regeneration: The stem cell that lies beneath. Bone, 70, 10-18. doi:10.1016/j.bone.2014.08.007 Saijo, M., Kitazawa, R., Nakajima, M., Kurosaka, M., Maeda, S., & Kitazawa, S. (2003). Heparanase mRNA expression during fracture repair in mice. Histochemistry and Cell Biology, 120(6), 493-503. doi:10.1007/s00418-003-0589-1 Sanderson, R. D. (2001). Heparan sulfate proteoglycans in invasion and metastasis. Seminars in Cell & Developmental Biology, 12(2), 89-98. doi:https://doi.org/10.1006/scdb.2000.0241 Sarrazin, S., Lamanna, W. C., & Esko, J. D. (2011). Heparan Sulfate Proteoglycans. Cold Spring Harbor Perspectives in Biology, 3(7), a004952. doi:10.1101/cshperspect.a004952 Schmid, G. J., Kobayashi, C., Sandell, L. J., & Ornitz, D. M. (2009). Fibroblast growth factor expression during skeletal fracture healing in mice. Developmental Dynamics, 238(3), 766-774. doi:10.1002/dvdy.21882 Shriver, Z., Capila, I., Venkataraman, G., & Sasisekharan, R. (2012). Heparin and Heparan Sulfate: Analyzing Structure and Microheterogeneity. Handbook of experimental pharmacology(207), 159-176. doi:10.1007/978-3-642-23056-1_8 Smits, P., Li, P., Mandel, J., Zhang, Z., Deng, J. M., Behringer, R. R., . . . Lefebvre, V. (2001). The Transcription Factors L-Sox5 and Sox6 Are Essential for Cartilage Formation. Developmental Cell, 1(2), 277-290. doi:https://doi.org/10.1016/S1534-5807(01)00003-X Stafford, H. J., Roberts, M. T., Oni, O. O. A., Hay, J., & Gregg, P. (1994). Localisation of bone-forming cells during fracture healing by osteocalcin immunocytochemistry: An experimental study of the rabbit tibia. Journal of Orthopaedic Research, 12(1), 29-39. doi:doi:10.1002/jor.1100120105 Sugahara, K., & Kitagawa, H. (2002). Heparin and Heparan Sulfate Biosynthesis. IUBMB Life, 54(4), 163-175. doi:doi:10.1080/15216540214928 Tsumaki, N., & Yoshikawa, H. (2005). The role of bone morphogenetic proteins in endochondral bone formation. Cytokine & Growth Factor Reviews, 16(3), 279-285. doi:https://doi.org/10.1016/j.cytogfr.2005.04.001 Ueta, C., Iwamoto, M., Kanatani, N., Yoshida, C., Liu, Y., Enomoto-Iwamoto, M., . . . Komori, T. (2001). Skeletal Malformations Caused by Overexpression of Cbfa1 or Its Dominant Negative Form in Chondrocytes. The Journal of Cell Biology, 153(1), 87-100. Uusitalo, H., Rantakokko, J., Ahonen, M., Jämsä, T., Tuukkanen, J., KäHäri, V. M., . . . Aro, H. T. (2001). A metaphyseal defect model of the femur for studies of murine bone healing. Bone, 28(4), 423-429. doi:http://dx.doi.org/10.1016/S8756-3282(01)00406-9 van Horssen, J., Wesseling, P., van den Heuvel, L. P. W. J., de Waal, R. M. W., & Verbeek, M. M. (2003). Heparan sulphate proteoglycans in Alzheimer's disease and amyloid-related disorders. The Lancet Neurology, 2(8), 482-492. doi:https://doi.org/10.1016/S1474-4422(03)00484-8 Vlodavsky, I., Beckhove, P., Lerner, I., Pisano, C., Meirovitz, A., Ilan, N., & Elkin, M. (2012). Significance of Heparanase in Cancer and Inflammation. Cancer Microenvironment, 5(2), 115-132. doi:10.1007/s12307-011-0082-7 Vreys, V., & David, G. (2007). Mammalian heparanase: what is the message? Journal of Cellular and Molecular Medicine, 11(3), 427-452. doi:10.1111/j.1582-4934.2007.00039.x Wang, L., Fuster, M., Sriramarao, P., & Esko, J. D. (2005). Endothelial heparan sulfate deficiency impairs L-selectin- and chemokine-mediated neutrophil trafficking during inflammatory responses. Nature Immunology, 6, 902. doi:10.1038/ni1233 https://www.nature.com/articles/ni1233 - supplementary-information Wendeberg, B. (1961). Mineral Metabolism of Fractures of the Tibia in Man Studied with External Counting of Sr85. Acta Orthopaedica Scandinavica, 32(sup52), 3-81. doi:10.3109/ort.1961.32.suppl-52.01 Yang, X., Ricciardi, B. F., Hernandez-Soria, A., Shi, Y., Camacho, N. P., & Bostrom, M. P. G. (2007). Callus mineralization and maturation are delayed during fracture healing in interleukin-6 knockout mice. Bone, 41(6), 928-936. doi:10.1016/j.bone.2007.07.022 Yang, Y., Topol, L., Lee, H., & Wu, J. (2003). Wnt5a and Wnt5b exhibit distinct activities in coordinating chondrocyte proliferation and differentiation. Development, 130(5), 1003-1015. Ye, S., Luo, Y., Lu, W., Jones, R. B., Linhardt, R. J., Capila, I., . . . McKeehan, W. L. (2001). Structural Basis for Interaction of FGF-1, FGF-2, and FGF-7 with Different Heparan Sulfate Motifs. Biochemistry, 40(48), 14429-14439. doi:10.1021/bi011000u Yip, V. L. Y., & Withers, S. G. (2004). Nature's many mechanisms for the degradation of oligosaccharides. Organic & Biomolecular Chemistry, 2(19), 2707-2713. doi:10.1039/B408880H Yoon, B. S., Ovchinnikov, D. A., Yoshii, I., Mishina, Y., Behringer, R. R., & Lyons, K. M. (2005). Bmpr1a and Bmpr1b have overlapping functions and are essential for chondrogenesis in vivo. Proceedings of the National Academy of Sciences of the United States of America, 102(14), 5062-5067. doi:10.1073/pnas.0500031102 Yoon, B. S., Pogue, R., Ovchinnikov, D. A., Yoshii, I., Mishina, Y., Behringer, R. R., &Lyons, K. M. (2006). BMPs regulate multiple aspects of growth-plate chondrogenesis through opposing actions on FGF pathways. Development, 133(23), 4667. Yu, K., Xu, J., Liu, Z., Sosic, D., Shao, J., Olson, E. N., . . . Ornitz, D. M. (2003). Conditional inactivation of FGF receptor 2 reveals an essential role for FGF signaling in the regulation of osteoblast function and bone growth. Development, 130(13), 3063. Zhou, X., Zhang, Z., Feng, J. Q., Dusevich, V. M., Sinha, K., Zhang, H., . . . de Crombrugghe, B. (2010). Multiple functions of Osterix are required for bone growth and homeostasis in postnatal mice. Proceedings of the National Academy of Sciences of the United States of America, 107(29), 12919-12924. doi:10.1073/pnas.0912855107 | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/71178 | - |
| dc.description.abstract | 骨癒合向來是熱門的研究議題，範圍涵蓋臨床上功能與巨觀的解剖構造的恢復以及細胞分子層面的變化。硫酸乙醯醣蛋白（Heparin sulfate proteoglycans, HSPGs）是普遍存在於生物體細胞表面和細胞外基質中的醣蛋白，參與許多生長因子的訊號傳遞。第三型硫酸乙醯肝素酶（heparinase III）是一種可以切割HSPGs上硫酸乙醯肝素（heparin sulfate, HS）的酵素，對於HSPG和其所調節的分子訊號有間接的影響。本實驗的目的為評估heparinase III作用於HS後對小鼠骨缺損癒合的影響。本實驗中小鼠為實驗動物模式，在其遠端股骨製造一直徑1 mm之圓柱狀骨缺損，利用連續給藥膠囊及導管分別將heparinase III和heparinase III緩衝液給到實驗組和控制組的骨缺損處，並在術後第1、4、7、14、21天犧牲小鼠，以微電腦斷層、組織學檢查、定量聚合酶鏈式反應、和免疫化學染色的方式評估癒合情況。實驗組和控制組間最顯著的差別在術後第1天的蝕骨細胞acid phosphatase化學染色結果以及術後第4天蝕骨細胞的Cd68基因表現量。Heparinase III處理的組別在上述的兩種評估中皆表現出顯著較高的蝕骨細胞數量與分佈。由本實驗的結果可以得知heparinase III不會影響骨癒合最終的形態結果，但在早期蝕骨細胞的聚集和骨重吸收的作用中應扮演著重要的角色。 | zh_TW |
| dc.description.abstract | The healing of bone tissuehas always been a popular researchtopic. Besides restorationof clinical functionand returning to a macroscopic normal anatomical structure, changes at the microscopic cellular and molecular level should also be investigated. Heparin sulfate proteoglycans(HSPGs) are found on cell surfaceand in extracellularmatrix, where they participatein many signaling pathways of different growth factors. It is postulated thatmodulating HSPGs may influencethe processof bone healing indirectly.Heparinase III derived from microorganismiscapable of cleavingthe heparansulfate (HS) chain on HSPGs. This study aims to evaluate the effectof heparinase III in bone healing in mouse model. Mice with a distal femur bone defect were used as the animal model. Mice were randomly assigned to either the control group receiving heparinase buffer or the experiment group receiving heparinase III in heparinase buffer. The mice were sacrificed at1, 4, 7, 14, 21 days post-injury, and micro-CT, histological exam, qPCR, and immunohistochemistrywere performedto evaluate bone healing. Results showedthat the main difference betweenthe two groups are acid phosphatase histochemistry results at 1 day post-injury and Cd68 qPCR results at 4 days post-injury, with heparinase III group showing significant higher osteoclastnumbers and distribution. These results indicate that heparinase III may not affectthe final outcomeof bone healing, but certainly play a role in the early stage of osteoclastrecruitmentand bone resorption. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-17T04:57:06Z (GMT). No. of bitstreams: 1 ntu-107-R04643007-1.pdf: 67216151 bytes, checksum: b8e601688f65d4d3a39fbcba2cc9386d (MD5) Previous issue date: 2018 | en |
| dc.description.tableofcontents | 口試委員會審定書 #
誌謝 I 中文摘要 II ABSTRACT III CONTENTS IV 圖次 VIII 表次 XI 第1章、 緒論 1 1.1 前言 1 1.2 研究動機 1 第2章、 文獻檢討 3 2.1 骨折癒合 3 2.1.1 骨化方式 3 2.1.2 骨癒合的生理 4 2.1.2.1 急性炎症反應 5 2.1.2.2 間質幹細胞聚集 5 2.1.2.3 軟骨痂和骨周邊硬骨痂的生成 5 2.1.2.4 血管新生及血管重建 6 2.1.2.5 軟骨痂的礦物化和重吸收 6 2.1.2.6 骨重塑 7 2.2 骨生成之相關機制與分子訊號 8 2.2.1 軟骨分化 8 2.2.2 生長板發育 9 2.2.3 造骨細胞生成 11 2.3 骨癒合的評估 13 2.4 硫酸乙醯肝素蛋白聚糖 14 2.4.1 結構及特性 14 2.4.2 功能 17 2.4.2.1 組織基底膜屏障 18 2.4.2.2 細胞訊號的傳遞與型態生成 19 2.4.2.3 組織的受傷與修復 19 2.4.2.4 HSPG的負面影響 20 2.4.3 硫酸乙醯肝素酶 21 第3章、 試驗研究 25 3.1 目的 25 3.2 前導實驗 26 3.3 材料與方法 30 3.3.1 實驗設計 30 3.3.2 實驗動物 30 3.3.3 植入式連續給藥膠囊 31 3.3.4 手術步驟 32 3.3.5 實驗動物之安樂死 33 3.3.6 骨缺損癒合程度的評估 33 3.3.6.1 微電腦斷層影像檢查 34 3.3.6.2 組織學檢查 35 3.3.6.3 定量聚合酶鏈式反應 (qPCR) 36 3.3.6.4 免疫化學染色 37 3.3.7 統計分析 38 第4章、 結果 39 4.1 影像學量化統計 39 4.2 組織學檢查結果 44 4.3 定量聚合酶鏈式反應結果 51 4.4 免疫化學染色結果 59 4.4.1 TRAP化學染色 59 4.4.2 Osteocalcin免疫化學染色 60 第5章、 討論 73 5.1 骨缺損癒合時的形態變化 73 5.2 骨缺損癒合時細胞分子層面之變化 75 5.3 HEPARINASE III對骨癒合的影響 78 5.4 實驗設計之限制 79 第6章、 結論 81 REFERENCES 82 | |
| dc.language.iso | zh-TW | |
| dc.subject | 硫酸乙醯肝素 | zh_TW |
| dc.subject | 骨癒合 | zh_TW |
| dc.subject | 硫酸乙醯醣蛋白 | zh_TW |
| dc.subject | 骨缺損 | zh_TW |
| dc.subject | 第三型硫酸乙醯肝素梅 | zh_TW |
| dc.subject | bone defect | en |
| dc.subject | Heparin sulfate proteoglycans | en |
| dc.subject | Heparinase III | en |
| dc.subject | heparan sulfate | en |
| dc.subject | bone healing | en |
| dc.title | 第三型硫酸乙醯肝素酶對小鼠骨癒合的影響 | zh_TW |
| dc.title | The Effect of Heparinase III in Bone Healing in Mouse Model | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 106-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.coadvisor | 劉逸軒 | |
| dc.contributor.oralexamcommittee | 武敬和,皇甫維君,梁碧惠 | |
| dc.subject.keyword | 硫酸乙醯醣蛋白,第三型硫酸乙醯肝素梅,硫酸乙醯肝素,骨缺損,骨癒合, | zh_TW |
| dc.subject.keyword | Heparin sulfate proteoglycans,Heparinase III,heparan sulfate,bone healing,bone defect, | en |
| dc.relation.page | 89 | |
| dc.identifier.doi | 10.6342/NTU201802008 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2018-07-27 | |
| dc.contributor.author-college | 獸醫專業學院 | zh_TW |
| dc.contributor.author-dept | 臨床動物醫學研究所 | zh_TW |
| 顯示於系所單位： | 臨床動物醫學研究所 | |
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