Pronost S, Segond N, Macro M, Rédini F, Penfornis H, Jullienne A, Moukhtar M S, Pujol J P
Laboratoire de Biochimie du Tissu Conjonctif, CJF INSERM 91-06, Faculté de Médecine, Caen, France.
Osteoarthritis Cartilage. 1995 Sep;3(3):147-55. doi: 10.1016/s1063-4584(05)80049-4.
Interleukin-1 receptor type I (IL-1RI) expression in cultured rabbit articular chondrocytes (RAC) was studied by reverse transcription-polymerase chain reaction (RT-PCR). A cDNA probe specific for the rabbit IL-1RI gene was constructed using primers derived from the sequence data of the human, murine and chick receptors. Transforming growth factor-beta 1 (TGF beta-1) was shown to transiently increase the level of expected 900-bp PCR product at 1 h of incubation and decrease the expression at 48 and 72 h with no effect at 24 h. In receptor binding assays using [125I]-IL-1 alpha, TGF beta decreased IL-1R bioactivity at all time points. These results suggest that TGF beta-induced down-regulation of IL-1 RI could be responsible for its ability to antagonize the effect of IL-1 and that TGF beta may have a role in the repair of articular cartilage.
采用逆转录-聚合酶链反应(RT-PCR)研究了培养的兔关节软骨细胞(RAC)中I型白细胞介素-1受体(IL-1RI)的表达。利用从人、小鼠和鸡受体的序列数据中获得的引物构建了兔IL-1RI基因特异性的cDNA探针。结果显示,转化生长因子-β1(TGFβ-1)在孵育1小时时可使预期的900bp PCR产物水平短暂升高,在48小时和72小时时使表达降低,而在24小时时无影响。在使用[125I]-IL-1α的受体结合试验中,TGFβ在所有时间点均降低IL-1R生物活性。这些结果表明,TGFβ诱导的IL-1RI下调可能是其拮抗IL-1作用的原因,且TGFβ可能在关节软骨修复中发挥作用。