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Analysis of the differentiation mechanism of human bone marrow derived osteoprogenitor cells

人骨髓源性骨祖细胞分化机制分析

基本信息

批准号：
12470304
负责人：
ENDO Naoto
金额：
$ 9.54万
依托单位：
NIIGATA UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2000
资助国家：
日本
起止时间：
2000 至 2001
项目状态：
已结题

项目摘要

Because we could not get enough amounts of human bone marrow-derived cells, rats were used in this project to analyze the differentiation me chanism of bone marrow-derived mesencymal cells.1) Establishment of animal model for osteonecrosis of femoral head. Steroid administration could not induce osteonecrosis in rat femoral heads. Since steroid possibly induces ischemia in femoral heads, we tried t o create new osteonecrosis model using rats. We succeeded to create osteonecrosis by cutting the joint capsule and dislocating the femoral he ad. We are now investigating the histological features of the necrosis model including necrotic area and apoptosis.2) Investigation of the bone and cartilage changes in the distal femur of tail-suspended rats. Steroid treated rats had no remarkable changes in bone and cartilage. Since unloading condition could induce osteopenia and fat degeneration i n bone, we changed the animal model to investigate bone and cartilage in tail-suspended rats whose hind limbs were exposed to unloading condition. Unloading induced calcification of articular cartilage and growth inhibition of epiphyseal plate, those were inhibited by intermittent administration of 1-34 human parathyroid hormone.3) Osteoblasitc and adipocytic differentiation of human bone marrow-derived mesenchymal cells inoculated into nude mice Bone marrow-derived mesenchymal cells were inoculated in nude mice. BMP2 induce bone formation, but not adipogenesis in the inoculated mesenchymal cells. These data were not consistent with the in vitro data in which BMP2 induced both osteogenesis and adipogenesis.

由于我们无法获得足够数量的人骨髓源性细胞，本项目采用大鼠来分析骨髓源性间充质细胞的分化机制。1)建立股骨头坏死动物模型。类固醇不能引起大鼠股骨头坏死。由于类固醇可能引起股骨头缺血，我们尝试用大鼠建立新的股骨头坏死模型。我们通过切开关节囊并使股骨脱臼成功地造成了骨坏死。我们正在研究坏死模型的组织学特征，包括坏死面积和细胞凋亡。2)悬尾大鼠股骨远端骨软骨变化的研究。类固醇治疗大鼠的骨骼和软骨没有明显的变化。由于卸荷条件可引起骨内骨质减少和脂肪变性，我们改变动物模型，观察后肢卸荷条件下悬尾大鼠骨和软骨的变化。卸载诱导的关节软骨钙化和骨骺板生长抑制，可通过间歇性给药1-34人甲状旁腺激素抑制。3)人骨髓间充质细胞接种裸鼠成骨细胞和脂肪细胞分化。在接种的间充质细胞中，BMP2诱导骨形成，但不诱导脂肪形成。这些数据与体外BMP2诱导成骨和脂肪生成的数据不一致。