Fukuda K, Asada S, Kumano F, Saitoh M, Otani K, Tanaka S
Department of Orthopaedic Surgery, Kinki University School of Medicine, Osaka, Japan.
J Lab Clin Med. 1997 Aug;130(2):209-15. doi: 10.1016/s0022-2143(97)90098-6.
Osteoarthrosis, a common pathway of joint deterioration, is caused by mechanical stress loaded on articular cartilage. We previously demonstrated the involvement of protein kinase C (PKC) in the development of osteoarthritis in vitro. In this study, we examined the effect of mechanical stress on chondrocyte metabolism and the activity of PKC in vitro. Low frequency and magnitude of cyclic tensile stretch loaded on chondrocytes increased proteoglycan synthesis. However, high frequency and magnitude of stress decreased its synthesis. In this condition, activity of PKC was reduced. These results suggest an involvement of PKC in the stress-mediated inhibition of proteoglycan synthesis.
骨关节炎是关节退变的常见途径,由加载在关节软骨上的机械应力引起。我们之前在体外证明了蛋白激酶C(PKC)参与骨关节炎的发展。在本研究中,我们检测了机械应力对体外软骨细胞代谢和PKC活性的影响。加载在软骨细胞上的低频率和低强度循环拉伸增加了蛋白聚糖的合成。然而,高频率和高强度的应力则降低了其合成。在这种情况下,PKC的活性降低。这些结果表明PKC参与了应力介导的蛋白聚糖合成抑制。