Cartilage damaging activities of fibronectin fragments derived from cartilage and synovial fluid
Cartilage damaging activities of fibronectin fragments derived from cartilage and synovial fluid
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DOI：
10.1053/joca.1998.0116
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发表时间：
1998-07-01
影响因子：
7
通讯作者：
Hui, F
中科院分区：
文献类型：
--
作者：
Homandberg, GA;Wen, C;Hui, F
目的：为了研究是否可以在骨关节炎（OA）或类风湿性关节炎患者的软骨中发现纤维连接蛋白片段（Fn-fs），或者可以从滑液中的纤维连接蛋白（Fn）或培养软骨基质中的Fn产生。也要确定是否软骨或滑液Fn-FS是活跃的，因此，可能有助于软骨损伤在vivo.Methods：Fn-FS的免疫化学鉴定软骨提取物从OA或类风湿性关节炎患者或在牛软骨培养与IL-1 α或在牛滑液处理与基质分解素-1（MMP-3）。通过使流体通过抗Fn柱并将所得流体添加到牛软骨培养物中以测量蛋白聚糖（PCT）降解来测试从OA滑液中去除Fn-fs的效果。明胶-琼脂糖凝胶纯化的Fns从牛血浆，滑液或软骨与MMP-3和Fn-fs的降解PG的测试在培养的cartilage.Results：从类风湿关节炎或OA患者的软骨提取物中含有一系列的Fn-fs。从OA滑液中去除Fn-fs显着降低了所产生的损害时，流体被添加到培养的软骨。向培养的软骨中加入IL-1 α或向滑液中加入MMP-3可增强Fn-fs的产生。Fn-fs，无论是来自牛血浆或滑液或软骨Fns，损坏的cartilage.Conclusions：这些数据表明，虽然Fn-fs可以产生在体内的滑液和Fn-fs中发现的OA滑液可能有助于在体内的软骨损伤，Fn-fs也可以产生在软骨和放大软骨损伤。因此，Fn-fs可能是软骨代谢的自分泌和旁分泌调节剂。
Objective: To investigate whether fibronectin fragments (Fn-fs), shown to damage cultured cartilage, can be found in cartilage from patients with osteoarthritis (OA) or rheumatoid arthritis, or can be generated from fibronectin (Fn) within synovial fluids or from Fn in the matrix of cultured cartilage. To also determine whether cartilage or synovial fluid Fn-fs are active and, thus, could contribute to cartilage damage in vivo.Methods: Fn-fs were immunochemically identified in cartilage extracts from patients with OA or rheumatoid arthritis or in bovine cartilage cultured with IL-1 alpha or in bovine synovial fluids treated with stromelysin-1 (MMP-3). The effect of removal of Fn-fs were OA synovial fluids was tested by passing fluids over an anti-Fn column and adding the resultant fluids to bovine cartilage cultures to measure proteoglycan (PCT) degradation. Gelatin-Sepharose purified Fns from bovine plasma, synovial fluid or cartilage were digested with MMP-3 and the Fn-fs tested for degradation of PG; in cultured cartilage.Results: Extracts of cartilage from patients with rheumatoid arthritis or with OA contained a range of Fn-fs. Removal of Fn-fs from OA synovial fluids significantly reduced the resultant damage when the fluids were added to cultured cartilage. Addition of IL-1 alpha to cultured cartilage or of MMP-3 to synovial fluids enhanced generation of Fn-fs. Fn-fs, whether derived from bovine plasma or synovial fluid or cartilage Fns, damaged cartilage.Conclusions: These data demonstrate that although Fn-fs could be generated in vivo within synovial fluids and Fn-fs found in OA synovial fluid may contribute to cartilage damage in vivo, Fn-fs could also be generated within cartilage and amplify cartilage damage. Thus, Fn-fs may be both autocrine and paracrine regulators of cartilage metabolism.