Mitsui K
Department of Orthopaedic Surgery, Jikei University, School of Medicine, Toyko, Japan.
Nihon Seikeigeka Gakkai Zasshi. 1987 Jun;61(6):681-93.
The purpose of this study was to clarify the mechanism of joint destruction in rheumatoid arthritis and osteoarthritis by observing the effects of the pathological synovial fluids on proteoglycan (PG) and collagen metabolism of chondrocytes. When chondrocytes from chick embryo were cultured with pathological synovial fluids, especially RA synovial fluid, biosynthesis of both proteoglycan and collagen of chondrocytes were found to increase in proportion to the amounts of pathological synovial fluids applied to the culture medium. Chondrocytes began to synthesize PG of small molecular size, approximately 70,000 in addition to PG of normal molecular size. It is noteworthy that the PG of small molecular size shows a shortening of the glycosaminoglycan link and core protein on undersulfation. These findings indicate that pathological synovial fluids disturb the biochemical regulation of the articular cartilage matrix by altering both PG and collagen metabolisms of chondrocytes.
本研究的目的是通过观察病理性滑膜液对软骨细胞蛋白聚糖(PG)和胶原蛋白代谢的影响,阐明类风湿性关节炎和骨关节炎中关节破坏的机制。当用病理性滑膜液,特别是类风湿性关节炎滑膜液培养鸡胚软骨细胞时,发现软骨细胞的蛋白聚糖和胶原蛋白的生物合成与添加到培养基中的病理性滑膜液量成比例增加。软骨细胞开始合成除正常分子大小的PG外,还有大约70,000的小分子大小的PG。值得注意的是,小分子大小的PG显示出糖胺聚糖连接的缩短和核心蛋白的硫酸化不足。这些发现表明,病理性滑膜液通过改变软骨细胞的PG和胶原蛋白代谢来干扰关节软骨基质的生化调节。