The inhibitory effect of disease-modifying anti-rheumatic drugs and steroids on gliostatin/platelet-derived endothelial cell growth factor production in human fibroblast-like synoviocytes
The inhibitory effect of disease-modifying anti-rheumatic drugs and steroids on gliostatin/platelet-derived endothelial cell growth factor production in human fibroblast-like synoviocytes
复制标题
DOI：
10.1007/s00296-005-0624-8
复制
发表时间：
2005-10-01
影响因子：
4
通讯作者：
Asai, K
中科院分区：
文献类型：
--
作者：
Kusabe, T;Waguri-Nagaya, Y;Asai, K
Gliostatin/血小板衍生的内皮细胞生长因子（GLS/PD-ECGF）已知具有血管生成和关节炎生成活性。本研究的目的是调查是否疾病缓解抗风湿药物（DMARDs）和类固醇参与GLS表达的调节。从类风湿性关节炎（RA）患者中获得的成纤维细胞样滑膜细胞（FLS）进行培养，并用白细胞介素（IL）-1 β（含或不含DMARD和类固醇）刺激。采用逆转录-聚合酶链反应和ELISA法测定GLS的表达水平。在培养的类风湿FLSs中，GLS mRNA的表达在IL-1 β刺激下显著增加。相比之下，金硫葡萄糖（AuTG）和地塞米松（DEX）治疗可降低IL-1 β刺激的FLS中GLS mRNA水平。这些发现表明，AuTG和DEX具有抗风湿活性，这是通过抑制GLS产生介导的。在我们的研究中，甲氨蝶呤（MTX）和柳氮磺胺吡啶（SSZ）对GLS水平均无显著影响。
Gliostatin/platelet-derived endothelial cell growth factor (GLS/PD-ECGF) is known to have both angiogenic and arthritogenic activities. The purpose of this study was to investigate whether disease-modifying anti-rheumatic drugs (DMARDs) and steroids are involved in the regulation of GLS expression. Fibroblast-like synoviocytes (FLSs) obtained from patients with rheumatoid arthritis (RA) were cultured and stimulated by interleukin (IL)-1 beta with or without DMARDs and steroids. The expression levels of GLS were determined using the reverse transcription-polymerase chain reaction and an ELISA. In cultured rheumatoid FLSs, the expression of GLS mRNA was significantly increased by stimulation with IL-1 beta. By contrast, GLS mRNA levels in IL-1 beta-stimulated FLSs were reduced by treatment with aurothioglucose (AuTG) and dexamethasone (DEX). These findings indicate that AuTG and DEX have anti-rheumatic activity, which is mediated via the suppression of GLS production. Neither methotrexate (MTX) nor sulfasalazine (SSZ) had a significant influence on GLS levels in our study.