Stimulation of procollagenase synthesis parallels increases in cellular procollagenase mRNA in human articular chondrocytes exposed to recombinant interleukin 1 beta or phorbol ester.
Stimulation of procollagenase synthesis parallels increases in cellular procollagenase mRNA in human articular chondrocytes exposed to recombinant interleukin 1 beta or phorbol ester.
复制标题
刺激原胶原酶合成与暴露于重组白细胞介素 1β 或佛波酯的人关节软骨细胞中细胞原胶原酶 mRNA 的增加平行。
DOI：
10.1016/s0006-291x(87)80006-2
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发表时间：
1987
影响因子：
3.1
通讯作者：
Angel,P
中科院分区：
文献类型：
--
作者：
Stephenson,ML;Goldring,MB;Birkhead,JR;Krane,SM;Rahmsdorf,HJ;Angel,P
白细胞介素1，主要是单核细胞的产物，通过间充质靶细胞如滑膜成纤维细胞和关节软骨细胞增加前胶原酶和前列腺素E2的合成和释放，一些佛波醇酯模拟了这种作用。为了确定这些反应的机制，在存在或不存在环加氧酶抑制剂吲哚美辛的情况下，将人关节软骨细胞的原代培养物与重组人白细胞介素1β或佛波酯佛波醇12-肉豆蔻酸酯13-乙酸酯预孵育。白细胞介素1β或佛波酯增加了前胶原酶的水平（胰蛋白酶活化后测定）和与[35 S]甲硫氨酸孵育的细胞对几种培养基蛋白的标记，与前列腺素合成无关。55 kD的蛋白免疫复合物与抗体前胶原酶的标记也增加。前胶原酶的合成增加是由前胶原酶mRNA的细胞水平增加引起的，用编码人前胶原酶的cDNA探针测定。因此，在炎症介质白细胞介素1的作用下，前胶原酶的合成增加，是在翻译前水平，也可能是在转录水平上受到控制的。
Interleukin 1, a product predominantly of monocytes, increases the synthesis and release of procollagenase and prostaglandin E2by mesenchymal target cells such as synovial fibroblasts and articular chondrocytes, an effect mimicked by some phorbol esters. In order to determine the mechanisms underlying these responses primary cultures of human articular chondrocytes were preincubated with recombinant human interleukin 1β or the phorbol ester, phorbol 12-myristate 13-acetate, in the presence or absence of the cyclooxygenase inhibitor, indomethacin. Interleukin 1β or phorbol ester increased the levels of procollagenase (assayed after trypsin activation) and the labeling of several medium proteins by cells incubated with [35S]methionine, independent of prostaglandin synthesis. The labeling of a 55 kD protein immunocomplexed with antibodies to procollagenase was also increased. The increased synthesis of procollagenase was paralleled by increased cellular levels of procollagenase mRNA, determined with a cDNA probe coding for human procollagenase. Thus the increased synthesis of procollagenase in response to the inflammatory mediator, interleukin 1, is controlled at a pretranslational level, possibly at the level of transcription.