Involbement of adhesion molecules in osteoclast formation
粘附分子参与破骨细胞形成
基本信息
- 批准号:05671540
- 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:1993
- 资助国家:日本
- 起止时间:1993 至 1994
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Osteoclast, the bone resorbing cell, is formed from hematopoietic precursors via cell-cell fusion. To evaluate the possibility that under certain specific conditions mannose residues may be expressed on the preosteoclast cell surface, we examined the action of some compound which bind terminal mannose specifically, on the farmation of osteoclast induced in the coculture of mouse spleen cells with mouse stromal cell, TMS,a process in which cell-cell fusion is involved.Osteoclast formation was inhibited by treatment of this coculture system with some terminal mannose-binding drug at the fusion evednt. Whith an interactive lazer cytometer ACAS570, fluorescein isothiocyanate labeled drug, which binds mannose residue specifically, was observed to bind osteolast progenitors at thefusion process between mononuclear preosteoclasts.These results suggest that mannose residues were expressed on outer membranes of monocytes under pathophysiological conditions and that they were involved in the osteoclast formation via cellular membrane fusiom events.
破骨细胞是由造血前体细胞通过细胞-细胞融合形成的骨吸收细胞。为了评估在某些特定条件下甘露糖残基可能在破骨细胞前体细胞表面表达的可能性,我们检测了某些特异性结合末端甘露糖的化合物对小鼠脾细胞与小鼠基质细胞TMS共培养中诱导的破骨细胞培养的作用,一种涉及细胞与细胞融合的过程。在融合发生时,用某些末端甘露糖结合药物处理该共培养系统可抑制破骨细胞的形成。用ACAS 570激光流式细胞仪观察到特异性结合甘露糖残基的异硫氰酸荧光素标记药物在单核前破骨细胞融合过程中与破骨祖细胞结合,提示在病理生理条件下,甘露糖残基表达于单核细胞外膜,并通过细胞膜融合事件参与破骨细胞的形成。
项目成果
期刊论文数量(30)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
T.Kurachi,I.Morita: "Expression of outer membranes of mannose residues,which are involved in osteoclast formation via cellular fusion" J.Biol.Chem.269. 17572-17576 (1994)
T.Kurachi,I.Morita:“甘露糖残基外膜的表达,通过细胞融合参与破骨细胞的形成”J.Biol.Chem.269。
- DOI:
- 发表时间:
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- 影响因子:0
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- 通讯作者:
K.Sakaguchi,I.Morita: "Eicosapentaenoic acid inhibits bone loss due to avariectomy in rats" PG.LT and EFA. 51. 51-55 (1994)
K.Sakaguchi,I.Morita:“二十碳五烯酸抑制大鼠因卵巢切除术引起的骨质流失”PG.LT 和 EFA。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
T.Kurachi, I.Morita et al.: "Expression on outher membranes of mannose residues which are involved in osteoclast formation via cell fusion events" J.Biol.Chem. 269. 17572-17576 (1994)
T.Kurachi、I.Morita 等人:“通过细胞融合事件参与破骨细胞形成的甘露糖残基外膜上的表达”J.Biol.Chem。
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- 发表时间:
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- 影响因子:0
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K.Sakaguchi,I.Morita: "Eicosapentaenoic acid inhibits bone loss due to avariectomy in rats" PG.LT.EFA.(in press).
K.Sakaguchi,I.Morita:“二十碳五烯酸抑制大鼠因卵巢切除术引起的骨质流失”PG.LT.EFA.(印刷中)。
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- 影响因子:0
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N.Suda,I.Morita etc.: "Partification of oxidative stress in the presence of osteoclasts differentiation" Biochim.Biophys.Acta. 1151. 318-323 (1993)
N.Suda,I.Morita 等:“破骨细胞分化中氧化应激的部分”Biochim.Biophys.Acta。
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MORITA Ikuo其他文献
MORITA Ikuo的其他文献
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Mechanism for maintenance of homeostasis of several functions by connexin 43
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20390470 - 财政年份:2008
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Analysis of pathology based on four-dimensional analysis of intracellular communication through gap junction and their development for therapy
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17209058 - 财政年份:2005
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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
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$ 1.34万 - 项目类别:
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Involvement of PPAR γ in senescence-induced osteoporosis
PPAR γ 参与衰老引起的骨质疏松症
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12671799 - 财政年份:2000
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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
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$ 1.34万 - 项目类别:
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Physiological role of prostaglandin H2 synthase-2 (COX-2) in bone metabolism
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08672119 - 财政年份:1996
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Grant-in-Aid for Scientific Research (C)
Isolation of osteoclast-forming factor produced by stromal cells and mechanism of osteoclast differentiation
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- 批准号:
03670864 - 财政年份:1991
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
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