Elucidation of molecular mechanism of alveolar bone remodeling induced by orthodontic force.

阐明正畸力诱导牙槽骨重塑的分子机制。

基本信息

  • 批准号:
    17592155
  • 负责人:
  • 金额:
    $ 2.24万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    2005
  • 资助国家:
    日本
  • 起止时间:
    2005 至 2006
  • 项目状态:
    已结题

项目摘要

We have performed three experiments to elucidate the molecular mechanism by which alveolar bone remodeling induced by orthodontic force. The role of prostaglandin E2 (PGE_2) in osteoclastic bone resorption was carefully examined in this program.Exp. 1 : PGE_2 synergistically enhances RANKL-induced osteoclastic differentiation of the precursor cells. We investigated the mechanisms of the stimulatory effect of PGE_2 on osteoclast differentiation. The stimulatory effect of PGE_2 on the RANKL-induced osteoclast differentiation of the precursor cells was mediated through EP2 and EP4. TAK1 acted as an adapter molecule linking PKA-induced signals and RANKL-and TNFα-induced such signals in osteoclast precursors. Furthermore, TAK1 is involved in the synergistic effect of cAMP/PKA signals on TNF receptor-and Toll-like receptor 4 (TLR4)-induced signaling pathways. The cAMP/PKA signal may enhance bone resorption induced by RANKL and TNFα through TAK1 in osteoclast precursors.Exp. 2 : PGE_2 itself … More has been shown to directly inhibit bone-resorbing activity of osteoclasts. We explored the mechanism of PGE_2 action in the osteoclastic differentiation of precursor cells. The stimulatory effect of PGE_2 on the RANKL-induced osteoclast differentiation of the precursor cells was mediated through EP2 and EP4. TAK1 acted as an adapter molecule linking PKA-induced signals and RANKL-and TNFα-induced such signals in osteoclast precursors. Furthermore, TAK1 is involved in the synergistic effect of cAMP/PKA signals on TNF receptor-and Toll like receptor 4 (TLR4)-induced signaling pathways. The cAMP/PKA signal may enhance bone resorption induced by RANKL and TNFα through TAK1 in osteoclast precursors.Exp. 3 : We explored the role of PGE_2 in human osteoclast differentiation in more detail. Unlike mouse macrophage cultures, PGE_2 strongly inhibited RANKL-induced osteoclast formation in human CD14^+ cell cultures. Human osteoclast progenitors produced a soluble unidentified factor(s) in response to PGE_2, which strongly inhibited RANKL-induced osteoclast formation in not only human CD14^+ cell cultures but also mouse macrophage cultures. These results suggest that COX-2 inhibitors may not be suitable therapeutic agents to suppress osteoclastic bone resorption in inflammatory bone diseases. Less
我们进行了三种阐明了牙槽骨重塑的分子机制。在该程序中,谨慎地检查了整骨骨骼中的Staglandin E2(PGE_2)。 PGE_2对pge_2的效应TNF受体和收费的受体4(TLR4)诱导的信号通路。整骨。将信号和RANKL和RANKL和RANKL和RANK1诱导的tak1涉及TAK1。在骨骼前体中,通过tak1诱导的骨骼和TNFα诱导。 S)对PGE_2的反应,不仅在人类CD14^+细胞培养物中抑制RANKL诱导的破骨细胞。骨骼疾病

项目成果

期刊论文数量(18)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Cephalometric study of elderly with nearly intact dental arches.
牙弓几乎完整的老年人的头影测量研究。
  • DOI:
  • 发表时间:
    2006
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Kataoka K. et al.;Misawa Y et al.;Kataoka K. et al.;Okafuji N et al.;Okafuji N et al.;Hagiwara Y. et al.;Hagiwara Y. et al.;Shimizu T et al.
  • 通讯作者:
    Shimizu T et al.
Nurse-like cells from patients with rheumatoid arthritis support survival of osteoclast precursors via macrophage-colony stimulating factor production.
来自类风湿性关节炎患者的护士样细胞通过巨噬细胞集落刺激因子的产生支持破骨细胞前体的存活。
  • DOI:
  • 发表时间:
    2005
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Nakamichi Y et al.;Tsukiyama K et al.;Itoh S et al.;Yamamoto Y et al.;Udagawa N et al.;Okumura S et al.;Nakamichi Y et al.;Tsukiyama K et al.;Itoh S et al.;Yamamoto Y et al.;Udagawa N et al.;Okumura S et al.;Takahashi N et al.;Yamaki M;Kobayashi Y;Kobayashi Y;Yang S;Take I;Tsuboi H
  • 通讯作者:
    Tsuboi H
Tissue reaction to poly (lactic-co-glycolic acid) copolymer membrane in rhBMP used rabbit experimental mandibular reconstruction
rhBMP 中聚乳酸-乙醇酸共聚物膜的组织反应用于兔实验性下颌骨重建
  • DOI:
  • 发表时间:
    2006
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Kataoka K. et al.;Misawa Y et al.;Kataoka K. et al.;Okafuji N et al.;Okafuji N et al.;Hagiwara Y. et al.;Hagiwara Y. et al.;Shimizu T et al.;Hagiwara Yukari et al.;Okafuji N et al.;Terao Yutaka;Okafuji N et al.;Hino Ayako;Shimizu T et al.;Okafuji N et al.
  • 通讯作者:
    Okafuji N et al.
Tissue reaction to poly (lactic-co-glycolic acid) copolymer membrane in rhBMP used rabbit experimental mandibular reconstruction.
rhBMP 中聚乳酸-乙醇酸共聚物膜的组织反应用于兔实验性下颌骨重建。
  • DOI:
  • 发表时间:
    2006
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Kataoka K. et al.;Misawa Y et al.;Kataoka K. et al.;Okafuji N et al.
  • 通讯作者:
    Okafuji N et al.
Expression of Notchl and Mathl in mandibular condyle cartilage in neonatal mice.
Notch1和Mathl在新生小鼠下颌髁突软骨中的表达。
  • DOI:
  • 发表时间:
    2005
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Kataoka K. et al.;Misawa Y et al.;Kataoka K. et al.;Okafuji N et al.;Okafuji N et al.;Hagiwara Y. et al.;Hagiwara Y. et al.;Shimizu T et al.;Hagiwara Yukari et al.;Okafuji N et al.;Terao Yutaka;Okafuji N et al.;Hino Ayako;Shimizu T et al.;Okafuji N et al.;片岡 宏介等;Shimizu T et al.
  • 通讯作者:
    Shimizu T et al.
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KURIHARA Saburo其他文献

KURIHARA Saburo的其他文献

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{{ truncateString('KURIHARA Saburo', 18)}}的其他基金

Degradation and generation of collagen from periodontal tissues incident to mechanical stress
机械应力引起的牙周组织胶原蛋白的降解和生成
  • 批准号:
    19592376
  • 财政年份:
    2007
  • 资助金额:
    $ 2.24万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Research for Cell Behavior of Osteoclasts Receiving Mechanical Pressure
机械压力下破骨细胞细胞行为的研究
  • 批准号:
    62570911
  • 财政年份:
    1987
  • 资助金额:
    $ 2.24万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)

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