Cawston T E, Ellis A J, Humm G, Lean E, Ward D, Curry V
Rheumatology Research Unit, Addenbrooke's Hospital, Cambridge, UK.
Biochem Biophys Res Commun. 1995 Oct 4;215(1):377-85. doi: 10.1006/bbrc.1995.2476.
Interleukin-1 (IL-1) and Oncostatin M (OM) induce a rapid and reproducible release of proteoglycan and collagen fragments from bovine nasal cartilage in culture. Over 90% of the total collagen was released by day 14 compared to a variable release with IL-1 alone. This release was accompanied by the appearance of collagenolytic activity in the medium that cleaved collagen specifically at the one quarter/three quarter position. Tissue inhibitor of metalloproteinases (TIMP-1) activity was low or absent in media from resorbing tissue. The breakdown of cartilage collagen could be prevented by the addition of BB94, a specific matrix metalloproteinase (MMP) inhibitor. These results suggest that T-cell/macrophage products within inflammed joints can interact with pro-inflammatory cytokines and lead to the rapid destruction of connective tissue collagen.
白细胞介素-1(IL-1)和制瘤素M(OM)可诱导培养的牛鼻软骨快速且可重复地释放蛋白聚糖和胶原蛋白片段。与单独使用IL-1时的可变释放相比,到第14天时,超过90%的总胶原蛋白被释放。这种释放伴随着培养基中胶原olytic活性的出现,该活性在四分之一/四分之三位置特异性切割胶原蛋白。金属蛋白酶组织抑制剂(TIMP-1)活性在吸收组织的培养基中较低或不存在。添加特异性基质金属蛋白酶(MMP)抑制剂BB94可防止软骨胶原蛋白的分解。这些结果表明,炎症关节内的T细胞/巨噬细胞产物可与促炎细胞因子相互作用,并导致结缔组织胶原蛋白的快速破坏。