Effect of mechanical stress loaded on the chondrocytes

虽然骨关节炎是关节组织承受机械应力导致关节恶化的常见途径之一，但其潜在机制尚不清楚。为了阐明这一问题，我们引入了Flexercell Strain Unit，使我们能够在软骨细胞上加载循环拉伸，并研究了软骨细胞代谢的变化。循环拉伸引起软骨细胞形态改变，并促进糖胺聚糖和硫酸角蛋白的释放。DNA合成显著增强。另一方面，循环拉伸拉伸明显减少了蛋白多糖的合成，蛋白激酶C抑制剂逆转了拉伸诱导的蛋白多糖合成抑制。此外，苯酚酯预处理消除了应激介导的蛋白多糖合成抑制。这些数据表明蛋白激酶C参与关节软骨细胞机械应力的信号转导。

Although osteoarthritis is one of the popular pathway of joint deterioration results from the mechanical stress loaded on the joint tisse, the underlying mechanism has not been clarified. To elucidate this problem, we introduced Flexercell Strain Unit which enable us to load cyclic tensile stretch on the chondrocytes and investigated the alteration of chondrocytes metabolisms. Cyclic tensile stretch caused morphological change of chondrocytes and enhanced glycosaminoglycan and keratan sulfate release. DNA synthesis was significantly enhanced. On the other hand, cyclic tensile stretch clearly reduced proteoglycan synthesis and inhibitors of protein kinase C reversed stretch-induced inhibition of proteoglycan synthesis. Furthermore, pretreatment of phorbol ester abolished stress-mediated inhibition of proteoglycan synthesis. These data indicate the involvement of protein kinase C in the signal transduction of the mechanical stress loaded on the articular chondrocytes.