Kim Y J, Grodzinsky A J, Plaas A H
Continuum Electromechanics Group, Laboratory for Electromagnetic and Electronic Systems, Department of Electrical Engineering and Computer Science, Massachusetts Institute of Technology, Cambridge, 02139, USA.
Arch Biochem Biophys. 1996 Apr 15;328(2):331-40. doi: 10.1006/abbi.1996.0181.
The differential effects of static compression and recovery from compression on biosynthesis and biosynthetic pathways of aggrecan, link protein, and hyaluronan were assessed. During compression, biosynthesis of aggrecan and link protein were inhibited to approximately 25 and approximately 40%, respectively, of free-swelling control levels. In marked contrast, hyaluronan synthesis was unaffected by static compression. After release from 12-h 50% static compression, aggrecan synthesis remained inhibited for up to 2.5 days; however, link protein synthesis completely recovered to free-swelling control levels within 8 h after release. Hyaluronan synthesis remained at control levels after release of compression. During compression, aggrecan core protein pool size was decreased, whereas the rate of processing into the proteoglycan form remained essentially the same as in free swelling control tissue. Four hours after release from compression, aggrecan core protein pool size remained small and the rate of intracellular processing of aggrecan had become slower than that of free swelling control tissue. Due to the altered core-protein processing kinetics, fewer but longer chondroitin sulfate chains were added to the core proteins. Sulfation was not markedly altered. The differential effects of static compression and release on the biosynthesis of aggrecan, link protein, and hyaluronan are similar to the changes in the biosynthetic pathways that are affected in response to IL-1 treatment, suggesting that the response to static compression is not a general inhibition of cellular activity, but appears to be part of a specific transduction mechanism.
评估了静态压缩及从压缩状态恢复对聚集蛋白聚糖、连接蛋白和透明质酸生物合成及生物合成途径的不同影响。在压缩过程中，聚集蛋白聚糖和连接蛋白的生物合成分别被抑制至自由膨胀对照水平的约25%和约40%。与之形成显著对比的是，透明质酸合成不受静态压缩的影响。在12小时50%静态压缩解除后，聚集蛋白聚糖合成在长达2.5天的时间内仍受抑制；然而，连接蛋白合成在解除压缩后8小时内完全恢复至自由膨胀对照水平。压缩解除后，透明质酸合成维持在对照水平。在压缩过程中，聚集蛋白聚糖核心蛋白池大小减小，而加工成蛋白聚糖形式的速率与自由膨胀对照组织基本相同。从压缩状态解除4小时后，聚集蛋白聚糖核心蛋白池大小仍然较小，且聚集蛋白聚糖的细胞内加工速率变得比自由膨胀对照组织慢。由于核心蛋白加工动力学发生改变，核心蛋白上添加的硫酸软骨素链数量减少但长度增加。硫酸化未发生明显改变。静态压缩及解除对聚集蛋白聚糖、连接蛋白和透明质酸生物合成的不同影响与白细胞介素-1处理时受影响的生物合成途径变化相似，这表明对静态压缩的反应并非对细胞活性的普遍抑制，而似乎是特定转导机制的一部分。
