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A STUDY OF THE REGULATORY MECHANISM OF CYTOKINES ON OSTEOCLASTIC BONE RESORPTION IN POSTMENOPAUSAL OSTEOPOROSIS

绝经后骨质疏松症破骨细胞骨吸收细胞因子调节机制的研究

基本信息

批准号：
08670250
负责人：
KITAZAWA Riko
金额：
$ 1.41万
依托单位：
KOBE UNIVERSITY SCHOOL OF MEDICINE
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1996
资助国家：
日本
起止时间：
1996 至 1997
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-08670250/
关键词：
postmenopausal osteoporosis osteoclast cytokines M-CSF stromal cell in situ hybridizatin

项目摘要

Osteoclasts are multinucleated cells derived from hematopoietic cells. Osteoblastic/stromal cell lineage is indispensable for osteoclastogenesis by producing cytokines (e.g.M-CSF) for the survival of precursor cells and via the direct cell-to-cell interaction essential for the terminal differentiation of osteoclast precursors.We have shown the possibility that estrogen difficiency affects on osteoblastic/stromal cells and indirectly causes the increase of the formation of osteoclast. In this study, at first we investigated the role of M-CSF on the generation of the osteoclast precursor population. Then we focused on the supporting mechanism of stromal cells via cell-to-cell interaction. We focused the phenomenon of the passage-dependent reduction of osteoclastogenesis in the co-culture system of mouse stromal cell line.ST2, and hemopoietic cells. We attempted to isolate the molecules of which gene expression is associated to the ability of supporting osteoclastogenesis.To assess the expression of cytokines and genes invloved in osteoclastogenesis on the bone tissues, we set up the system of in situ hybridization using decalcified bone specimen. We have presented our data at various international as well as domestic meetings, and publish a lot of scientific papaers for academic jurnals.

破骨细胞是源自造血细胞的多核细胞。成骨细胞/基质细胞谱系通过产生细胞因子（如m - csf）来维持前体细胞的存活，并通过直接的细胞间相互作用来实现破骨细胞前体细胞的最终分化，这对于破骨细胞的形成是必不可少的。我们已经证明雌激素缺乏可能影响成骨细胞/基质细胞，并间接导致破骨细胞形成的增加。在这项研究中，我们首先研究了M-CSF在破骨细胞前体群体产生中的作用。然后，我们重点研究了基质细胞通过细胞间相互作用的支持机制。我们研究了小鼠基质细胞系共培养系统中破骨细胞生成的传代依赖性减少现象。ST2和造血细胞。我们试图分离出与支持破骨细胞生成能力相关的基因表达分子。为了评估骨组织中细胞因子和破骨细胞发生相关基因的表达，我们建立了脱钙骨标本原位杂交系统。我们在各种国际和国内会议上展示了我们的数据，并在学术期刊上发表了大量的科学论文。