| Project/Area Number |
15592173
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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 |
Orthodontic/Pediatric dentistry
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| Research Institution | Meikai University |
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Principal Investigator |
KIYOMURA Masaru Meikai University, School of Dentistry, Orthodontics, Assistant Professor, 歯学部, 助手 (10337503)
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| Co-Investigator(Kenkyū-buntansha) |
MANO Mikiko Meikai University, School of Dentistry, Orthodontics, Associate Professor, 歯学部, 講師 (00333005)
TOMOMURA Akito Meikai University, School of Dentistry, Biochemistry, Professor, 歯学部, 教授 (60188810)
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| Project Period (FY) |
2003 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2005: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2004: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2003: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | Orthodontics / Protease / Calcium / Bone / カルデクリン / 骨代謝 / 血清カルシウム降下因子 / 骨粗鬆症 / 遺伝子治療 |
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| Research Abstract |
Although it is a principal object how teeth movement is performed in orthodontics, the teeth movement means a bone-remodeling. Caldecrin, a serine protease of approx. 28 kDa purified from the pancreas, is hypocalcemic factor expressed with high frequency in cases of acute pancreatitis. It has been reported that the bone-resorbing activity of mature osteoclasts was significantly inhibited by caldecrin ; however, the effect of caldecrin on osteoclastgenesis is not clear. Therefore, in this study, the effect of caldecrin on osteoclastgenesis in the mouse was investigated. Wild-type and protease-deficient caldecrin dose-dependently inhibited the differentiation from mouse bone marrow cells to osteoclasts (tartrate-resistant acid phosphatase (TRAP) activity, TRAP-positive cell formation) elicited by tumor necrosis factor-α (TNF-α) or receptor activator of NF-κB ligand (RANKL) stimulation. Caldecrin did not affect macrophage colony formation, osteoclast precursor formation nor cell proliferation. Caldecrin inhibited RANKL-stimulated the transcriptional activity of NFATc1 (nuclear translocation and DNA binding) and increase of the expression of NFATc1mRNA. In addition, it inhibited the activity of calcineurin. These results suggest further potential that osteoclastgenesis is suppressed, effect of caldecrin to osteoclast precursor cells, by the regulation of both the transcriptional activation and mRNA expression of NFATc1 via the Ca^<2+>/calcineurin system.
These results suggest that local treatment of caldecrin relates to potential uses in the field of orthodontics.
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