Regulation of interleukin-1β-induced interleukin-6 gene expression in human fibroblast-like synoviocytes by glucocorticoids
Regulation of interleukin-1β-induced interleukin-6 gene expression in human fibroblast-like synoviocytes by glucocorticoids
复制标题
DOI：
10.1093/oxfordjournals.jbchem.a022231
复制
发表时间：
1998-12-01
影响因子：
2.7
通讯作者：
Okudaira, H
中科院分区：
文献类型：
--
作者：
Miyazawa, K;Mori, A;Okudaira, H
白细胞介素-6（IL-6）参与类风湿性关节炎（RA）的发病机制。在本研究中，研究了糖皮质激素和IL-1 β对成纤维细胞样滑膜细胞（FLS）中IL-6基因表达的调节。合成和天然糖皮质激素，即，地塞米松（DEX）和氢化可的松（HC）分别浓度依赖性地抑制人FLS的IL-6蛋白质合成和基因表达。地塞米松可显著降低IL-6基因的转录速率，但不影响IL-6 mRNA的稳定性。IkappaB α通路似乎不参与地塞米松抑制IL-1 β刺激的人FLS中IL-6基因表达的作用。
Involvement of interleukin-6 (IL-6) in the pathogenesis of rheumatoid arthritis (RA) has recently been demonstrated. In the present study, the regulation of IL-6 gene expression by glucocorticoids and IL-1 beta in fibroblast-like synoviocytes (FLSs) was investigated. Both synthetic and natural glucocorticoids, i.e., dexamethasone (DEX) and hydrocortisone (HC), respectively, concentration-dependently inhibited protein production and gene expression of IL-6 by human FLSs, The effect of DEX was dependent on de novo protein synthesis. DEX significantly reduced the rate of IL-6 gene transcription without affecting the stability of IL-6 mRNA, The IkappaBalpha pathway seemed not to be involved in DEX-mediated inhibition of IL-6 gene expression in IL-1 beta-stimulated human FLSs, These findings suggest that glucocorticoids suppress IL-6 gene transcription by an as yet undefined mechanism.