Effect of mechanical stress loaded on the chondrocytes

机械应力对软骨细胞的影响

• 批准号: 06671495
• 负责人: FUKUDA Kanji
• 金额: $ 0.7万
• 依托单位: Kinki University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1994
• 资助国家: 日本
• 起止时间: 1994 至 1995
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-06671495/
• 关键词: chondrocytes; mechanical stress; protein kinase C; osteoarthritis; 関節軟骨; メカニカルストレス; 変形性関節症

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.

骨关节炎是关节组织在机械应力作用下发生退化的常见途径之一，但其机制尚不清楚。为了阐明这个问题，我们引入Flexercell应变单元，使我们能够对软骨细胞施加周期性拉伸载荷，并研究软骨细胞代谢的变化。周期性牵张可引起软骨细胞形态学改变，并促进软骨细胞糖胺聚糖和硫酸角质素的释放。DNA合成显著增强。另一方面，周期性拉伸明显减少蛋白聚糖合成和蛋白激酶C的抑制剂逆转拉伸诱导的蛋白聚糖合成抑制。此外，佛波酯的预处理废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参与了加载在关节软骨细胞上的机械应力的信号转导。

项目成果

福田寛二: "周期的牽引負荷による軟骨代謝の変化" 日整会誌. 68. s1400-s1401 (1994)

Kanji Fukuda：“循环牵引负荷引起的软骨代谢变化”日本自治学会杂志 68. s1400-s1401 (1994)。

K. Fukuda,et al: "Zonal difference of nitric oxide synthesis with interleukin-1 in bovine chondrocyte" Inflammation Research. 44. 434-437 (1995)

K. Fukuda 等人：“牛软骨细胞中白介素 1 与一氧化氮合成的区域差异”炎症研究。

K.Fukuda: "Interleukin-1 inhibits keratan sulfate production by rabbit chondrocytes : Possible role of prostaglandin E2." Inflammation Res. 44. 178-181 (1995)

K.Fukuda：“Interleukin-1 抑制兔软骨细胞产生硫酸角质素：前列腺素 E2 的可能作用。”

K.Fukuda,et al.: "Hyaluronic acid inhibits interleukin-l-induced cartilage degradation" Japanese Journal of Rheumatology. (In press).

K.Fukuda 等人：“透明质酸抑制白细胞介素-1 诱导的软骨退化”日本风湿病杂志。

K. Fukuda,et al: "Hyaluronic acid inhibits interleukin-1-induced cartilage degradation" Jpn. J. Rheumatology. 5. 345-353 (1995)

K. Fukuda 等人：“透明质酸抑制白细胞介素 1 诱导的软骨退化”Jpn。