转化生长因子β1调节分化的人关节软骨细胞中金属蛋白酶组织抑制剂-1的表达。
Transforming growth factor beta 1 regulates tissue inhibitor of metalloproteinases-1 expression in differentiated human articular chondrocytes.
作者信息
Günther M, Haubeck H D, van de Leur E, Bläser J, Bender S, Gütgemann I, Fischer D C, Tschesche H, Greiling H, Heinrich P C
机构信息
Institut für Biochemie, Rheinisch-Westfälischen Technischen Hochschule (RWTH), Aachen, Germany.
出版信息
Arthritis Rheum. 1994 Mar;37(3):395-405. doi: 10.1002/art.1780370314.
OBJECTIVE
To investigate the role of interleukin-6 (IL-6) and transforming growth factor beta 1 (TGF beta 1) in the regulation of tissue inhibitor of metalloproteinases-1 (TIMP-1) synthesis in human articular chondrocytes.
METHODS
Articular cartilage was obtained from human knee joints 24 hours after death. Chondrocytes were isolated by collagenase digestion and embedded in low-gelling-temperature agarose. After stimulation by cytokines, total RNA was isolated and analyzed by Northern blotting. TIMP-1 protein levels were determined using a competitive enzyme-linked immunosorbent assay.
RESULTS
Human chondrocytes in agarose culture expressed messenger RNA (mRNA) for the IL-6 receptor (gp80) and its signal-transducing subunit gp130. In contrast to the findings in a previous study, IL-6 did not stimulate TIMP-1 expression in these cells, whereas TGF beta 1 was an important inducer of TIMP-1 mRNA and protein synthesis.
CONCLUSION
Our findings suggest that TGF beta 1 has a protective effect on the extracellular matrix of human articular chondrocytes.
目的
研究白细胞介素-6（IL-6）和转化生长因子β1（TGFβ1）在调控人关节软骨细胞中金属蛋白酶组织抑制剂-1（TIMP-1）合成中的作用。
方法
在人死后24小时从膝关节获取关节软骨。通过胶原酶消化分离软骨细胞并包埋于低熔点琼脂糖中。细胞因子刺激后，分离总RNA并通过Northern印迹法进行分析。使用竞争性酶联免疫吸附测定法测定TIMP-1蛋白水平。
结果
琼脂糖培养的人软骨细胞表达IL-6受体（gp80）及其信号转导亚基gp130的信使核糖核酸（mRNA）。与先前研究结果相反，IL-6未刺激这些细胞中TIMP-1的表达，而TGFβ1是TIMP-1 mRNA和蛋白合成的重要诱导剂。
结论
我们的研究结果表明，TGFβ1对人关节软骨细胞的细胞外基质具有保护作用。
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