Jikko A, Wakisaka T, Iwamoto M, Hiranuma H, Kato Y, Maeda T, Fujishita M, Fuchihata H
Department of Oral and Maxillofacial Radiology, Faculty of Dentistry, Osaka University, 1-8 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Cell Biol Int. 1998;22(9-10):615-21. doi: 10.1006/cbir.1998.0304.
Interleukin-6 (IL-6) levels are markedly increased in the synovial fluid of patients with rheumatoid arthritis or osteoarthritis. However, the effects of IL-6 on proliferation and proteoglycan metabolism in articular cartilage are not known. We demonstrated here the effects of human recombinant (hr) IL-6 on proliferation and proteoglycan metabolism in rabbit articular chondrocyte cultures. In vitro, these cells proliferated and produced abundant extracellular matrices. We found that 1-10 ng/ml of hrIL-6 inhibited proliferation to approximately 65% of control levels and suppressed colony formation induced by bFGF in soft agarose. The same concentration of hrIL-6 depressed proteoglycan synthesis to approximately 60% of control levels. Moreover, hrIL-6 significantly enhanced proteoglycan degradation induced by hrIL-1beta, although hrIL-6 alone did not affect proteoglycan degradation. These findings suggest that IL-6 is a negative regulator for chondrocyte proliferation and articular cartilage metabolism.
类风湿性关节炎或骨关节炎患者的滑液中白细胞介素-6(IL-6)水平显著升高。然而,IL-6对关节软骨增殖和蛋白聚糖代谢的影响尚不清楚。我们在此证明了重组人(hr)IL-6对兔关节软骨细胞培养物中增殖和蛋白聚糖代谢的影响。在体外,这些细胞增殖并产生丰富的细胞外基质。我们发现,1-10 ng/ml的hrIL-6可将增殖抑制至对照水平的约65%,并抑制碱性成纤维细胞生长因子(bFGF)在软琼脂糖中诱导的集落形成。相同浓度的hrIL-6将蛋白聚糖合成降低至对照水平的约60%。此外,hrIL-6显著增强了hrIL-1β诱导的蛋白聚糖降解,尽管单独的hrIL-6并不影响蛋白聚糖降解。这些发现表明,IL-6是软骨细胞增殖和关节软骨代谢的负调节因子。