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Adiponectin-mediated changes in effector cells involved in the pathophysiology of rheumatoid arthritis

机译：脂联素介导的影响类风湿关节炎病理生理的效应细胞变化

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摘要

ObjectiveRheumatoid arthritis (RA) is associated with increased production of adipokines, which are cytokine-like mediators that are produced mainly in adipose tissue but also in synovial cells. Since RA synovial fibroblasts (RASFs), lymphocytes, endothelial cells, and chondrocytes are key players in the pathophysiology of RA, this study was undertaken to analyze the effects of the key adipokine adiponectin on proinflammatory and prodestructive synovial effector cells.MethodsLymphocytes were activated in part prior to stimulation. All cells were stimulated with adiponectin, and changes in gene and protein expression were determined by Affymetrix and protein arrays. Messenger RNA and protein levels were confirmed using semiquantitative reverse transcription–polymerase chain reaction (PCR), real-time PCR, and immunoassays. Intracellular signal transduction was evaluated using chemical signaling inhibitors.ResultsAdiponectin stimulation of human RASFs predominantly induced the secretion of chemokines, as well as proinflammatory cytokines, prostaglandin synthases, growth factors, and factors of bone metabolism and matrix remodeling. Lymphocytes, endothelial cells, and chondrocytes responded to adiponectin stimulation with enhanced synthesis of cytokines and various chemokines. Additionally, chondrocytes released increased amounts of matrix metalloproteinases. In RASFs, adiponectin-mediated effects were p38 MAPK and protein kinase C dependent.ConclusionOur previous findings indicated that adiponectin was present in inflamed synovium, at sites of cartilage invasion, in lymphocyte infiltrates, and in perivascular areas. The findings of the present study indicate that adiponectin induces gene expression and protein synthesis in human RASFs, lymphocytes, endothelial cells, and chondrocytes, supporting the concept of adiponectin being involved in the pathophysiologic modulation of RA effector cells. Adiponectin promotes inflammation through cytokine synthesis, attraction of inflammatory cells to the synovium, and recruitment of prodestructive cells via chemokines, thus promoting matrix destruction at sites of cartilage invasion.
机译：目的类风湿关节炎（RA）与脂肪因子的产生有关，脂肪因子是细胞因子样介质，主要在脂肪组织和滑膜细胞中产生。由于RA滑膜成纤维细胞（RASFs），淋巴细胞，内皮细胞和软骨细胞是RA病理生理的关键因素，因此本研究旨在分析关键脂联素脂联素对促炎性和破坏性滑膜效应细胞的作用。在刺激之前。用脂联素刺激所有细胞，并通过Affymetrix和蛋白质阵列确定基因和蛋白质表达的变化。使用半定量逆转录-聚合酶链反应（PCR），实时PCR和免疫测定法确认信使RNA和蛋白质水平。结果使用化学信号抑制剂评估细胞内信号转导。结果脂联素刺激人的RASF主要诱导趋化因子，促炎细胞因子，前列腺素合成酶，生长因子以及骨代谢和基质重塑因子的分泌。淋巴细胞，内皮细胞和软骨细胞对脂联素刺激产生反应，并增强了细胞因子和各种趋化因子的合成。另外，软骨细胞释放出增加量的基质金属蛋白酶。在RASF中，脂联素介导的作用是p38 MAPK和蛋白激酶C依赖性的。结论我们以前的发现表明，脂联素存在于发炎的滑膜，软骨浸润部位，淋巴细胞浸润和血管周区域。本研究的发现表明，脂联素诱导人RASF，淋巴细胞，内皮细胞和软骨细胞中的基因表达和蛋白质合成，支持脂联素参与RA效应细胞的病理生理调节的概念。脂联素通过细胞因子合成，炎症细胞对滑膜的吸引以及经由趋化因子募集前消灭性细胞而促进炎症，从而促进软骨侵袭部位的基质破坏。

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  • 来源
    《Arthritis & Rheumatism》 |2010年第10期|p.2886-2899|共14页
  • 作者

    Klaus W. Frommer; Birgit Zimmermann; Florian M. P. Meier; Dirk Schröder; Matthias Heil; Andreas Schffler; Christa Büchler; Jürgen Steinmeyer; Fabia Brentano; Steffen Gay; Ulf Müller-Ladner; Elena Neumann;

  • 作者单位

    Justus-Liebig-University Giessen and Kerckhoff-Klinik, Bad Nauheim, Germany;

    Justus-Liebig-University Giessen and Kerckhoff-Klinik, Bad Nauheim, Germany;

    Justus-Liebig-University Giessen and Kerckhoff-Klinik, Bad Nauheim, Germany;

    Justus-Liebig-University Giessen and Kerckhoff-Klinik, Bad Nauheim, Germany;

    Max-Planck Institute for Heart and Lung Research, Bad Nauheim, Germany;

    University of Regensburg, Regensburg, Germany;

    University of Regensburg, Regensburg, Germany;

    University Hospital Giessen and Marburg, Giessen, Germany;

    University Hospital Zurich, Zurich, Switzerland;

    University Hospital Zurich, Zurich, Switzerland;

    Justus-Liebig-University Giessen and Kerckhoff-Klinik, Bad Nauheim, Germany;

    Justus-Liebig-University Giessen and Kerckhoff-Klinik, Bad Nauheim, Germany;

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