Gliostatin/platelet-derived endothelial cell growth factor as a clinical marker of rheumatoid arthritis and its regulation in fibroblast-like synoviocytes.

Gliostatin/platelet-derived endothelial cell growth factor as a clinical marker of rheumatoid arthritis and its regulation in fibroblast-like synoviocytes.
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胶质抑素/血小板源性内皮细胞生长因子作为类风湿性关节炎的临床标志物及其在成纤维细胞样滑膜细胞中的调节。

DOI:
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发表时间:
1997
期刊:
British Journal of Rheumatology
影响因子:
--
通讯作者:
T. Kato
T. Kato
中科院分区:
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文献类型:
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作者:
Y. Waguri;T. Otsuka;I. Sugimura;N. Matsui;K. Asai;A. Moriyama;T. Kato

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本研究的目的是评价胶质抑素/血小板衍生内皮细胞生长因子(GLS-PD-ECGF)与类风湿关节炎(RA)其他临床标志物的一致性,以明确其在RA发病机制中复杂的细胞因子网络中的作用机制。免疫分析系统被用来定量实验室和临床样本中的GLS或细胞因子水平。逆转录-聚合酶链式反应检测GLS的表达水平。滑液中GLS水平与IL-1、IL-8水平呈正相关。血清GLS水平的系列数据较好地反映了4例典型类风湿关节炎患者临床病程中疾病活动性的变化。在培养的成纤维细胞样滑膜细胞中,肿瘤坏死因子-α(TNF-α)、IL-1、IL-6和IL-8诱导GLS表达。综上所述,我们的结果表明,血清GLS水平是RA的一个有用的临床标志物,主要来源于细胞因子刺激的滑膜细胞。
The objective was to assess the congruity of gliostatin/platelet-derived endothelial cell growth factor (GLS PD-ECGF) with other clinical markers of rheumatoid arthritis (RA) and to define its molecular mechanism of action in the complicated cytokine network during RA pathogenesis. Immunoassay systems were used to quantify GLS or cytokine levels in laboratory and clinical samples. Expression levels of GLS were determined by reverse transcription-polymerase chain reaction methods. The GLS levels in synovial fluid were correlated with interleukin-1 (IL-1) and IL-8. The serial data of serum GLS levels reflected well changes in the disease activity during the clinical course of four representative patients with RA. In cultured fibroblast-like synoviocytes, tumour necrosis factor-alpha (TNF-alpha), IL-1, IL-6 and IL-8 induced GLS expression. In conclusion, our results suggest that the serum GLS level, mostly derived from cytokine-stimulated synoviocytes, was a useful clinical marker of RA.
DOI: 10.1126/science.2544996
发表时间: 1989-07-07
期刊: SCIENCE
影响因子: 56.9
作者:
LEE, PL;JOHNSON, DE;WILLIAMS, LT
通讯作者: WILLIAMS, LT
DOI: 10.4049/jimmunol.147.7.2187
发表时间: 1991-10
影响因子: 4.4
作者:
A. Koch;S. Kunkel;J. Burrows;H. Evanoff;G. K. Haines;R. Pope;R. Strieter
通讯作者: A. Koch;S. Kunkel;J. Burrows;H. Evanoff;G. K. Haines;R. Pope;R. Strieter