Isolation of osteoclast-forming factor produced by stromal cells and mechanism of osteoclast differentiation

基质细胞产生的破骨细胞形成因子的分离及破骨细胞分化机制

基本信息

  • 批准号:
    03670864
  • 负责人:
  • 金额:
    $ 1.34万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)
  • 财政年份:
    1991
  • 资助国家:
    日本
  • 起止时间:
    1991 至 1992
  • 项目状态:
    已结题

项目摘要

I have succeeded to isolate the stromal cell line, which can support osteoclast formation from spleen cells and named as TMS-14 and 14. Using these stromal cells we studied the mechanism of osteoclast formation. As a result, osteoclast formation will be necessary for cAMP elevation in the stromal cells and an activation of A-kinase. And also the contact between spleen cells and stromal cells is also needed. Therefore, we next studied what adhesion molecule is important for osteoclast formation. In stromal cells ICAM-1 was expressed and in osteoclast progenitor cells LFA-1 and ICAM-1 were expressed. The antibodies for ICAM-1 and LFA-1 was added in the osteoclast formation system, the formation of osteoclast was significantly suppressed. However, the inhibition rate was only 50%. These results suggest that the other adhesion molecules was involved for osteoclast formation.Stromal cells release osteoclast formation-stimulating factors as well as inhibiting factors. We failed to isolate the stimulators, but succeeded to characterize the inhibitory factors for osteoclast formation. The inhibitor was released from osteoblasts as well as stromal cells and the moleculr weight will be over 10000. The inhibitor can be regulated by some anti-osteoporosis drugs. This means that some drugs for osteoporosis affects via a production of this inhibitor for osteoclast formation.
我成功地从脾细胞中分离出了能支持破骨细胞形成的基质细胞系,命名为TMS-14和14。利用这些基质细胞,我们研究了破骨细胞形成的机制。因此,破骨细胞的形成对于基质细胞中cAMP的升高和A-激酶的活化是必要的。脾细胞与基质细胞之间的接触也是必需的。因此,我们接下来研究了什么粘附分子对破骨细胞的形成是重要的。基质细胞表达ICAM-1,破骨细胞祖细胞表达LFA-1和ICAM-1。在破骨细胞形成体系中加入ICAM-1和LFA-1抗体,破骨细胞的形成受到明显抑制。然而,抑制率仅为50%。这些结果表明,破骨细胞的形成可能与其他粘附分子有关,基质细胞不仅能释放破骨细胞形成的抑制因子,还能释放破骨细胞形成的刺激因子。我们未能分离刺激因子,但成功地描述了破骨细胞形成的抑制因子。该抑制剂可从成骨细胞和基质细胞中释放,分子量超过10000。该抑制剂可被一些抗骨质疏松药物调节。这意味着一些骨质疏松症药物通过产生这种破骨细胞形成抑制剂来影响。

项目成果

期刊论文数量(15)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
K.Toriyama,I.Morita S.Murota: "The existence of distinct class of prostaglandin E2 receptors mediating adenylate cyclase and phospholipase C pathways in osteoblastic clone,MC3T3ーE1" Prostagl.Leukotri.and EFA.
K.Toriyama、I.Morita S.Murota:“在成骨细胞克隆 MC3T3-E1 中存在介导腺苷酸环化酶和磷脂酶 C 途径的不同类别的前列腺素 E2 受体”Prostagl.Leukotri. 和 EFA。
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    0
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I.Morita et al: "Iprifavone inhibits murine osteoclast formation in vitro" Calcified Tissue International. 51. S7- 10 (1992)
I.Morita 等人:“Iprifavone 在体外抑制小鼠破骨细胞形成”Calcified Tissue International。
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    0
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K. Toriyama, I. Morita, Y. Seyama, S. Yamashita, S. Murota: "Variation of increases in free cytosolic calcium ion induced by prostaglandin E2 in mouse osteoblast clone, MC3T3-E1" J. Bone and Mineral Research. 9. 34-38 (1991)
K. Toriyama、I. Morita、Y. Seyama、S. Yamashita、S. Murota:“小鼠成骨细胞克隆 MC3T3-E1 中前列腺素 E2 诱导的游离胞质钙离子增加的变化”J. 骨与矿物质研究。
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    0
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I. Morita, K. Sakaguchi, T. Kurachi, S. Murota: "Ipriflavone inhibits murine osteoclast formation in vitro" Calcified Tissue International. 51. s7-s10 (1992)
I. Morita、K. Sakaguchi、T. Kurachi、S. Murota:“伊普黄酮在体外抑制小鼠破骨细胞形成”钙化组织国际。
  • DOI:
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  • 影响因子:
    0
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  • 通讯作者:
K.Toriyama,I.Morita: "Variation of increase in free cytosolic calcium ion induced by prostaglandin E2 in mouse osteoblast clone,MC3T3ーE1" J Bone Mineral Metab. 9. 34-38 (1991)
K.Toriyama,I.Morita:“小鼠成骨细胞克隆 MC3T3-E1 中前列腺素 E2 诱导的游离胞质钙离子增加的变化”J Bone Mineral Metab. 9. 34-38 (1991)
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MORITA Ikuo其他文献

MORITA Ikuo的其他文献

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{{ truncateString('MORITA Ikuo', 18)}}的其他基金

Development of novel therapies for myopia by printing technology
利用印刷技术开发近视新疗法
  • 批准号:
    25670728
  • 财政年份:
    2013
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for Challenging Exploratory Research
A novel periodontal tissue regeneration method using a printing technology
一种利用打印技术的牙周组织再生新方法
  • 批准号:
    24390442
  • 财政年份:
    2012
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Development of tissue engineering for three-dimensional tissue regeneration
三维组织再生组织工程的发展
  • 批准号:
    22659354
  • 财政年份:
    2010
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for Challenging Exploratory Research
Mechanism for maintenance of homeostasis of several functions by connexin 43
连接蛋白 43 维持多种功能稳态的机制
  • 批准号:
    20390470
  • 财政年份:
    2008
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Analysis of pathology based on four-dimensional analysis of intracellular communication through gap junction and their development for therapy
基于间隙连接细胞内通讯四维分析的病理学分析及其治疗发展
  • 批准号:
    17209058
  • 财政年份:
    2005
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for Scientific Research (A)
Regulation of angiogenesis by PEDF, anti-angiogenic factor, for controlling Oral Diseases
通过 PEDF(抗血管生成因子)调节血管生成,以控制口腔疾病
  • 批准号:
    15390558
  • 财政年份:
    2003
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Involvement of PPAR γ in senescence-induced osteoporosis
PPAR γ 参与衰老引起的骨质疏松症
  • 批准号:
    12671799
  • 财政年份:
    2000
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Identification of inhibitor of osteoclastogenesis
破骨细胞生成抑制剂的鉴定
  • 批准号:
    10671734
  • 财政年份:
    1998
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Physiological role of prostaglandin H2 synthase-2 (COX-2) in bone metabolism
前列腺素 H2 合酶 2 (COX-2) 在骨代谢中的生理作用
  • 批准号:
    08672119
  • 财政年份:
    1996
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Involbement of adhesion molecules in osteoclast formation
粘附分子参与破骨细胞形成
  • 批准号:
    05671540
  • 财政年份:
    1993
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)

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Runx2阐明软骨细胞向成骨细胞转分化的分子机制
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