| Project/Area Number |
13672161
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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 |
矯正・小児・社会系歯学
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| Research Institution | Nagasaki University |
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Principal Investigator |
HOTOKEZAKA Hitoshi Nagasaki University, Department of Developmental and Reconstructive Medicine, Instructor, 大学院・医歯薬学総合研究科, 助手 (90199513)
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| Co-Investigator(Kenkyū-buntansha) |
NEMOTO Takayuki Nagasaki University, Department of Developmental and Reconstructive Medicine, Professor, 大学院・医歯薬学総合研究科, 教授 (90164665)
KITAMURA Akira Nagasaki University, Department of Developmental and Reconstructive Medicine, Associate professor, 大学院・医歯薬学総合研究科, 助教授 (30094767)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,900,000)
Fiscal Year 2002: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2001: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | cytokine / stress protein / signaltransduction / odontoclasts / osteoclasts / MEK / ERK / rootresorption / HSP / IL-1 / IL-6 / TNF-alpha / リコンビナント / 歯肉溝浸出液 |
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| Research Abstract |
The effect of stress proteins on osteoclast (odontoclast) differentiation of preosteoclast cells (monocyte/macrophage) which was used as a in vitro model experiment of root resorption in this study. When the cells were stumulated with 100μg/ml recombinant human HSP70 and HSP90, proinflammatory cytokines (IL-1 beta, IL-6, TNF-alpha) were not induced as well as that the osteoclast differentiation was not affected. Root resorption is thought to be induced by odontoclast that is differentiated from precursor hematopeetic stem cells with the stimulation of RANKL (Receptor Activator of Nuclear Flactor kappa B Ligand) expressed on osteoblasts. Stimulation of RANKL is known to induce phospholylation of signal transduction molecules, MAPK (Mitogen Activated Ptotein Kinase) including p38 MARK and ERK (Extracellular ignal-Regulated Kinase). Then the cells were stimulated with stress proteins to investigate if the stress proteins modulate the phosphorylation of those signal transduction molecules. However, any change of phosphorylation was observed with the stimulation of stress proteins. We concluded that HSP70 and HSP90 do no induce proinflammatory cytokines in monocyte/macrophage and do not affect the osteoclast differentiation. However during in this study, a signal trasnduction pathway (MEK/ERK) was found to be very important in osteoclast differentiation. The inhibitors of MEK markedly induced osteoclast differentiation in precursor cell line, which is the first report of the inhibition of signal transduction stimulates osteoclastogenesis.
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