Immunolocalization of selected cytokines and proteases in canine articular cartilage after transarticular loading.
Immunolocalization of selected cytokines and proteases in canine articular cartilage after transarticular loading.
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经关节加载后犬关节软骨中选定细胞因子和蛋白酶的免疫定位。
DOI：
10.1002/jor.1100110302
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
ThompsonJr,RC
中科院分区：
文献类型：
--
作者：
Pickvance,EA;OegemaJr,TR;ThompsonJr,RC
细胞因子和蛋白酶被认为在软骨的破坏和骨关节炎的发展中起作用。本研究的目的是记录白细胞介素-1 β（IL-1β）、肿瘤坏死因子-α（TNF-α）、基质溶解素（MMP-3）、纤连蛋白和硫酸软骨素硫酸化模式改变的时序参与。对犬髌骨进行闭合关节撞击以诱发骨关节炎。在第2、12、24和52周处死动物。髌骨损伤包括软骨浅表区和钙化软骨-骨界面区的裂缝、钙化软骨区的垂直阶梯状骨折以及软骨深层和浅表区裂缝周围的蛋白多糖丢失。使用抗生物素蛋白-生物素免疫组织化学，用IL-1β、TNF-α、MMP-3、纤连蛋白抗体和单克隆抗体3-B-3对这些标本进行染色。在2周时获得的4份标本中，有3份在软骨浅表和移行区的裂缝周围显示出IL-1β、TNF-α、MMP-3和纤连蛋白的强细胞和弱基质染色模式。在深层裂纹中未观察到一致的染色模式。在12、24或52周时获得的标本均未对这些抗体进行染色。在任何标本中均未发现3-B-3抗体的异常硫酸化染色。第52周时获得的样本显示阶梯骨折愈合，蛋白聚糖丢失得到填补。该模型可能反映了创伤后髌骨的短期软骨变化;因此，细胞因子和蛋白酶仅短暂升高。
Cytokines and proteases are thought to play a role in the destruction of cartilage and the development of osteoarthritis. The purpose of this study was to document chronological involvement of interleukin‐1 beta (IL‐1β), tumor necrosis factor‐alpha (TNF‐α), stromelysin (MMP‐3), fibronectin, and alteration in the chondroitin sulphate sulfation pattern. Canine patellae underwent a closed‐joint impact to induce the development of osteoarthritis. The animals were killed at 2, 12, 24, and 52 weeks. The patellar damage included cracks in the superficial zone of cartilage and the zone of the calcified cartilage‐bone interface, vertical step‐off fractures in the zone of calcified cartilage, and loss of proteoglycan around the cracks in the deep and superficial zones of cartilage. With avidin‐biotin immunohistochemistry, these specimens were stained with antibodies to IL‐1β, TNF‐α, MMP‐3, fibronectin, and altered proteoglycan sulfate with the monoclonal antibody 3‐B‐3. Three of the four specimens obtained at 2 weeks demonstrated a strong cellular and weak matrix staining‐pattern for IL‐1β, TNF‐α, MMP‐3, and fibronectin around the cracks in the superficial and transitional zones of cartilage. No consistent staining pattern was noted in the cracks in the deep zone. None of the specimens obtained at 12, 24, or 52 weeks stained for these antibodies. No staining for the abnormal sulfation with the 3‐B‐3 antibody was evident in any specimen. The specimens obtained at 52 weeks showed healing of the step‐off fractures and a filling‐in of the proteoglycan loss. This model probably reflects the short‐term cartilaginous changes in the patella after trauma; thus, only transient elevations in the cytokines and proteases were evident.