Cs-Szabó G, Melching L I, Roughley P J, Glant T T
Rush Medical College at Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois 60612, USA.
Arthritis Rheum. 1997 Jun;40(6):1037-45. doi: 10.1002/art.1780400607.
To determine the steady-state messenger RNA (mRNA) levels and corresponding protein contents of major matrix components in osteoarthritic (OA) cartilage.
Steady-state levels of gene-specific mRNA (relative to GAPDH) were measured by quantitative polymerase chain reaction (PCR), and the relative levels of the corresponding proteins were determined by Western blotting.
All mRNA levels and corresponding protein contents of aggrecan and versican (hyaluronan-binding large proteoglycans), decorin, biglycan, fibromodulin, and lumican (small proteoglycans), and link protein were higher in OA cartilage samples than in age-matched normal samples. The ratio of increase, however, was different for each component. The mRNA and protein levels of biglycan, decorin, and fibromodulin increased synchronously, whereas message for link protein and lumican were several-fold higher than expected by their measured protein contents. Versican was also detected in OA cartilage; however, the versican protein content was associated with a relatively low mRNA level.
The expression of matrix components was increased in chondrocytes of OA cartilage, especially the expression of small proteoglycans, most likely due to the repair processes. A discoordinate gene expression accompanied with imbalanced accumulation of noncollagenous matrix components may contribute to the disorganization of the cartilage and the development of OA processes.
测定骨关节炎（OA）软骨中主要基质成分的稳态信使核糖核酸（mRNA）水平及相应蛋白质含量。
采用定量聚合酶链反应（PCR）测定基因特异性mRNA的稳态水平（相对于甘油醛-3-磷酸脱氢酶），通过蛋白质印迹法测定相应蛋白质的相对水平。
OA软骨样本中聚集蛋白聚糖和多功能蛋白聚糖（透明质酸结合性大蛋白聚糖）、核心蛋白聚糖、双糖链蛋白聚糖、纤维调节蛋白和亮蛋白聚糖（小蛋白聚糖）以及连接蛋白的所有mRNA水平和相应蛋白质含量均高于年龄匹配的正常样本。然而，各成分的增加比例有所不同。双糖链蛋白聚糖、核心蛋白聚糖和纤维调节蛋白的mRNA和蛋白质水平同步增加，而连接蛋白和亮蛋白聚糖的信使核糖核酸水平比根据其测定的蛋白质含量预期的高几倍。在OA软骨中也检测到多功能蛋白聚糖；然而，多功能蛋白聚糖的蛋白质含量与相对较低的mRNA水平相关。
OA软骨细胞中基质成分的表达增加，尤其是小蛋白聚糖的表达，很可能是由于修复过程所致。非胶原蛋白基质成分积累失衡伴随的基因表达失调可能导致软骨结构紊乱和OA病程发展。
