Etipathogenesis of osteoarthritis and cartilage proteoglycan.

骨关节炎和软骨蛋白多糖的发病机制。

基本信息

批准号：
60480337
负责人：
IWATA Hisashi
金额：
$ 3.52万
依托单位：
Nagoya University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1985
资助国家：
日本
起止时间：
1985 至 1986
项目状态：
已结题

项目摘要

The research includes morphological, biochemical and immunological work about the proteoglycan in articular cartilage.Light and electron microscopic observations on the structure of epiphyseal cartilages in the cmd/cmd mice, which had genetically failed to synthesize cartilage-characteristic proteoglycan but were normal in type <II> collagen synthesis, showed apparent abnormalities of collagen fibrils: e.g. increase in the diameter, appearance of periodic banding patterns and bundle-formation of collagen fibrils. These findings suggest that cartilage-characteristic proteoglycan (Cartilage PG) normally limits the lateral growth of collagen fibrils and affects collagen fibrillogenesis in vivo.Chondrocytes from the cmd/cmd cartilage cultured in vitro produced nodules with greatly reduced extracellular matrix. Immunofluorescence staining revealed that the nodules of mutant cells differed from the normal in lacking cartilage PG and in uneven and reduced deposition of type <II> collagen. Exogenously added cartilage PG prepared from either normal mouse cartilage or Swarm rat chondrosarcoma to the culture medium was incorporated exclusively into the extracellular matrices of the nodules, with a concurrent correction of the abnormal distribution pattern of type <II> collagen. The incorporation of cartilage PG into the matrix was disturbed by hyaluronic acid or decasaccharide.The results indicate that the intact from of cartilage PG is required for specific incorporation into the chondrocyte nodules, and further suggest that cartilage PG plays a regulatory role in the assembly of the matrix macromolecules.

这项研究包括有关关节软骨中蛋白聚糖的形态，生化和免疫学工作。光明和电子显微镜观察CMD/CMD小鼠的周期性软骨结构的结构，这些小鼠的结构在遗传学上未能合成软骨蛋白质蛋白质，但在遗传上表现出正常的合成性<ii>正常的合成性<ii>正常<ii>胶原原纤维：例如直径增加，周期性带模式的出现以及胶原纤维的束形成。这些发现表明，软骨特性蛋白聚糖（软骨PG）通常限制胶原蛋白原纤维的侧向生长，并影响体内的胶原蛋白原纤维生成。从CMD/CMD植物中培养的绒毛性软骨的粘膜细胞大大降低了外胞外核酸内膜，并产生了大量的。免疫荧光染色表明，突变细胞的结节与缺乏软骨pg的正常状况不同，<ii>胶原蛋白的不均和沉积减少。将从正常小鼠软骨或大鼠软骨肉瘤制成的外源性软骨PG专门掺入结节的细胞外基质中，并同时校正型胶原型<ii>胶原蛋白的异常分布模式。将软骨PG掺入基质中受到透明质酸或Decasaccharide的干扰。结果表明，要具体掺入软骨细胞结节中，需要从软骨PG的完整性PG进行完整，并进一步表明软骨PG在基质中的基质Macromoleceles的组装中起调节作用。