| Project/Area Number |
17591910
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Okayama University |
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Principal Investigator |
NAGATSUKA Hitoshi Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Oral Pathology and Medicine, Associate Professor, 大学院医歯薬学総合研究科, 助教授 (70237535)
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| Co-Investigator(Kenkyū-buntansha) |
NAGAI Noriyuki Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Oral Pathology and Medicine, Professor, 大学院医歯薬学総合研究科, 教授 (90085770)
MEHMET Gunduz Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Oral Pathology and Medicine, Assistant, 大学院医歯薬学総合研究科, 助手 (70333507)
TSUJIGIWA Hidetsugu Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Oral Pathology and Medicine, Assistant, 大学院医歯薬学総合研究科, 助手 (70335628)
TAMAMURA Ryo Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Oral Pathology and Medicine, Assistant, 大学院医歯薬学総合研究科, 助手 (00403494)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2006: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2005: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Odontogenic tumor / Heparanase / Ameloblastoma / Immunohistochemistry / In situ hybridization / Protein expression / Cell differentiaton / Heparan sulfate / 遺伝子 |
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| Research Abstract |
Heparan sulphate proteoglycan (HSPG) are important extracellular matrix molecules that play critical roles in cell-cell and cell-matrix interactions. Most of the biological functions are conferred by the multitude of bioactive molecules sequestered on heparan sulphate sugar chains. Heparanase is a specific endoglycosidase enzyme that selectively degrades HSPG. The degradation of HSPG by heparanase can cause the release of bioactive molecules for important cellular functions in developmental and pathological processes and also the profound decrease in extracellular matrix and basement membrane integrity.
HSPG were ubiquitously detected in the tooth germ with strongest intensities in the stratum intermedium cells and the dental papilla cells whereas heparanase immunoexpression was quite limited to the growing cervical loop areas. All odontogenic tumors studied, showed stronger immunoreaction to heparanase than in the tooth germ. In ameloblastoma and adenomatoid odontogenic tumor. HSPG and heparanase were localized primarily in the neoplastic epithelium without significant staining in the mature fibrous stroma while in ameloblastic fibroma; both epithelial and mesenchymal cells were reactive. In the case of ameloblastic carcinoma, the localization of HSPG shifted to the stromal tissues accompanied by strong epithelial staining to heparanase. From the results, we suggest that: 1) increased immunolocalization of heparanase molecules may be a responsible factor for the neoplastic growth of odontogenic tissues, 2) the main function of heparanase in the normal odontogenic tissue may be local modulation of HSPG and HS bound bioactive molecules, 3) the function of heparanase is locally and tightly regulated in normal tooth germ and also to some extent in benign odontogenic tumors, 4) change in localization of HSPG and increased immunoexpression of heparanase in neoplastic cells, may represent the malignant progression of ameloblastoma to ameloblastic carcinoma.
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