| Project/Area Number |
16591896
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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 |
Pathobiological dentistry/Dental radiology
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| Research Institution | Nihon University |
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Principal Investigator |
MAENO Masao Nihon University, School of Dentistry, Professor, 歯学部, 教授 (60147618)
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| Co-Investigator(Kenkyū-buntansha) |
OGISO Bunnai Nihon University, School of Dentistry, Associate Professor, 歯学部, 助教授 (70147643)
MOTOHASHI Masafumi Nihon University, School of Dentistry, Associate Professor, 歯学部, 助教授 (90102615)
SUZUKI Naoto Nihon University, School of Dentistry, Associate Professor, 歯学部, 助教授 (10226532)
TANABE Natsuko Nihon University, School of Dentistry, Assistant, 歯学部, 助手 (10409097)
関 みつ子 日本大学, 歯学部, 助手 (20226640)
加藤 英美 日本大学, 歯学部, 助手 (90297838)
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| Project Period (FY) |
2004 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2004: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | dental radicular cysts / interleukin-1 / osteoblasts / osteoclasts / bone formation / bone resorption / M-CSF / RANKL / インターロイキン-1α / 破骨細胞前駆細胞 / RANKL / 炭酸脱水酵素II型 / カテプシンK / マトリックス金属プロテアーゼ-9 / プロスタグランジン / マトリックスメタロプロテアーゼ / マトリックスプロテアーゼ組織インヒビター / 石灰化nodule形成 / アルカリホスファターゼ / I型コラーゲン / 骨シアロタンパク / オステオポンチン |
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| Research Abstract |
Interleukin-1 (IL-1) is a proinflammatory cytokine that is a potent stimulator of bone resorption and an inhibitor of bone formation. We examined the effect of IL-1α on cell proliferation, alkaline phosphatase (ALPase) activity, mineralized nodule formation, and the expression of extracellular matrix proteins in rat osteosarcoma cell lines. Our results suggested that IL-1α suppresses osteogenesis through a decrease in ALPase and type I collagen production by osteoblasts. We also examined the effect of the inflammatory mediator IL-1α on the expression of macrophage colony-stimulating factor (M-CSF), osteoprotegerin (OPG), and prostaglandin E_2 (PGE_2) in rat osteoblasts, and the indirect effect of IL-1α on the formation of osteoclast-like cells. Our results suggested that IL-1α stimulated the formation of osteoclast-like cells via an increase in M-CSF and PGE_2 production, and a decrease in OPG production by osteoblasts. IL-1 plays key roles in altering bone matrix turnover. This turnov
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er is regulated by matrix metalloproteinases (MMPs), tissue inhibitor of matrix metalloproteinases (TIMPs), and the plasminogen activation system, including tissue-type plasminogen activator (tPA), urokinase-type plasminogen activator (uPA), and plasminogen activator inhibitor type-1 (PAI-1). Our results suggested that IL-1 a stimulate bone matrix turnover by increasing MMPs, tPA, and uPA production and decreasing PAI-1 production by osteoblasts, and incline the turnover to the resolution. M-CSF and RANK ligand (RANKL) are essential and sufficient for osteoclast differentiation. We examined the effects of IL-1α or RANKL and/or M-CSF in the presence of IL-1α on the expression of carbonic anhydrase II (CA II), cathepsin K, MMP-9,RANK, M-CSF receptor (c-fms), and c-fos transcription factor using RAW264.7 cells as osteoclast precursors. Our results indicated that the expression of CA II, cathepsin K, and MMP-9 in RAW264.7 cells is not induced by M-CSF, but by RANKL in the presence of IL-1α. Less
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