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Research the origin of cells that contribute to the repair of osteochondral defect and application this for the acceleration of the tissue repair.

研究有助于骨软骨缺损修复的细胞起源，并将其应用于加速组织修复。

基本信息

批准号：
21591953
负责人：
WAKITANI Shigeyuki
金额：
$ 2.91万
依托单位：
Mukogawa Women's University (2011)Osaka City University (2009-2010)
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2009
资助国家：
日本
起止时间：
2009 至 2011
项目状态：
已结题

项目摘要

We examined the possibility that cells circulating in peripheral blood participated in a natural repair process of the joint bone and cartilage injury by using green fluorescent protein transgenic transgenic(GFP) rat. In this study, we used the parabiosis model of GFP rat and wild one. Two weeks after parabiosis operation, vascular communication was confirmed by flow cytometry analysis. 1.5 mm diameter and 1.0 mm depth osteochondral defect was made in patella groove of femoral bone. Histrogical examination was done at 1, 2, 4, 24 weeks after surgery. In the early phase after the surgery, there were both GFP negative and positive cells in the defects of both rats of parabiosis. GFP positive chondrocytes was confirmed partly in the repair tissue of the wild rat of parabiosis. In the late phase after the surgery, the repaired defect was occupied by cells originated from the adjacent tissue not from the peripheral blood. The rate of cells originated from the peripheral blood was about 30-40% in the repair tissue at 1 week after surgery. While at 24 weeks after surgery that was about 0-7%. From these results, it is confirmed that cells circulating in peripheral blood contributed to repair of osteochondral defects in joint especially in early phase not only supplying the factors needed for repair but also supplying the repair cells.When injected granulocyte colony stimulating factor(G-CSF ; 150μg/kg pre day for 5 days) to rats, the nucleated cells in blood increased. After the cells increase, we made 1.5mm diameter and 1.0 mm depth osteochondral defect and observed up to 24 weeks. The repair of subchondral bone was accelerated although that of cartilage did not. To obtain better repair, we increased the nucleated cell more by injecting G-CSF for 14 days. After the cells increased more, we made defects and observed for 2 weeks. When we compared the repair of the preceding method with the new one, there were no significant differences between them.

我们利用绿色荧光蛋白转基因（GFP）大鼠研究了外周血循环细胞参与关节骨软骨损伤自然修复过程的可能性。本研究采用GFP大鼠与野生大鼠的异种共生模型。异种共生术后2周，流式细胞术分析证实血管连通。在股骨髌骨沟处制造直径1.5 mm、深度1.0 mm的骨软骨缺损。分别于术后1、2、4、24周行组织学检查。术后早期，异种共生大鼠的缺损中均有GFP阴性细胞和阳性细胞。在异种共生野生大鼠的修复组织中发现部分GFP阳性软骨细胞。在手术后期，修复的缺损被来自邻近组织的细胞所占据，而不是来自外周血。术后1周修复组织中来自外周血的细胞比例约为30-40%。而在手术后24周，这一比例为0-7%。这些结果证实，外周血循环细胞不仅提供修复所需的因子，而且提供修复细胞，对关节骨软骨缺损尤其是早期骨软骨缺损的修复有一定的作用。给大鼠注射粒细胞集落刺激因子（G-CSF, 150μg/kg，预注射5 d）后，血中有核细胞增多。细胞增殖后，制作直径1.5mm、深度1.0 mm的骨软骨缺损，观察24周。软骨修复无明显促进作用，但软骨下骨的修复有明显促进作用。为了获得更好的修复，我们通过注射G-CSF使有核细胞增加14天。待细胞增多后，制作缺损，观察2周。当我们将前一种修复方法与新方法进行比较时，两者之间没有显著差异。