Sugiura N, Iwasaki S, Aoki S, Hori Y, Sakurai K, Suzuki S, Kimata K
Institute for Molecular Science of Medicine, Aichi Medical University, Japan.
Int J Exp Pathol. 1995 Oct;76(5):369-79.
In rheumatoid arthritis, pannus formation resulting from synovial inflammation is a major factor in cartilage destruction. The ability of arthritic synovial cells to undergo pannus formation depends upon their initial adhesion to the partially deformed cartilage surfaces. Our recent studies using various lipid-derivatized glycosaminoglycans have revealed a preeminent inhibitory activity of phosphatidyl ethanol amine-derivatized chondroitin sulphate (CS-PE) toward cell-matrix adhesion. Here we evaluate whether CS-PE may protect articular cartilage from pannus extension in different in vitro and in vivo model systems using Escherichia coli 0:14-induced arthritis in rabbits and the articular cartilage explants, synovial tissues, and synovial cells obtained from them. These studies showed that CS-PE suppressed the in vivo pannus-like extension on cartilage surfaces, as well as the in vitro extension of the synovial cell layer on both CS-PE treated culture plates and cartilage explants. The results suggest that native chondroitin sulphate proteoglycans in the surface of normal articular cartilage play an important role in protecting the tissues from pannus extension and that the CS-PE immobilized onto partially eroded cartilage can mimic the inhibitory action of native chondroitin sulphate proteoglycans.
在类风湿性关节炎中,滑膜炎症导致的血管翳形成是软骨破坏的主要因素。关节炎滑膜细胞形成血管翳的能力取决于它们最初对部分变形的软骨表面的粘附。我们最近使用各种脂质衍生化糖胺聚糖的研究表明,磷脂酰乙醇胺衍生化硫酸软骨素(CS-PE)对细胞-基质粘附具有卓越的抑制活性。在此,我们使用大肠杆菌0:14诱导的兔关节炎以及从兔身上获取的关节软骨外植体、滑膜组织和滑膜细胞,在不同的体外和体内模型系统中评估CS-PE是否可以保护关节软骨免受血管翳扩展的影响。这些研究表明,CS-PE抑制了软骨表面的体内血管翳样扩展以及滑膜细胞层在CS-PE处理的培养板和软骨外植体上的体外扩展。结果表明,正常关节软骨表面的天然硫酸软骨素蛋白聚糖在保护组织免受血管翳扩展方面发挥着重要作用,并且固定在部分侵蚀软骨上的CS-PE可以模拟天然硫酸软骨素蛋白聚糖的抑制作用。