Synergy between adiponectin and interleukin-1β on the expression of interleukin-6, interleukin-8, and cyclooxygenase-2 in fibroblast-like synoviocytes.
Synergy between adiponectin and interleukin-1β on the expression of interleukin-6, interleukin-8, and cyclooxygenase-2 in fibroblast-like synoviocytes.
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DOI：
10.3858/emm.2012.44.7.049
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发表时间：
2012-07-31
影响因子：
12.8
通讯作者：
Kim KS
中科院分区：
文献类型：
--
作者：
Lee YA;Choi HM;Lee SH;Yang HI;Yoo MC;Hong SJ;Kim KS
为了确定脂联素与促炎细胞因子白细胞介素（IL）-1β联合是否对关节炎关节炎症过程中促炎介质的产生具有协同作用，用脂联素、IL-1β及其组合处理类风湿性关节炎（RA）患者的滑膜细胞24 h。收集培养上清液，并通过酶联免疫吸附测定法分析IL-6、IL-8、前列腺素E2（PGE 2）、血管内皮生长因子（VEGF）和基质金属蛋白酶（MMPs）的水平。研究脂联素介导的细胞内信号通路，以阐明其协同作用的分子机制。研究了关节炎患者滑液中促炎介质与脂联素的关系。脂联素与IL-1β协同激活RA成纤维细胞样滑膜细胞中IL-6、IL-8和PGE 2的表达; VEGF、MMP-1和MMP-13的水平没有协同刺激。脂联素和IL-1β均增加脂联素受体1和IL-1受体1的表达。然而，脂联素和IL-1β并不能协同支持IκB-α的降解或NF-κB的核转位。协同增加的基因表达被NF-κB抑制剂MG 132显著抑制。支持体外结果，IL-6和IL-8水平与RA患者关节滑液中的脂联素呈正相关，但与骨关节炎（OA）无关。总之，脂联素和IL-1β可能通过未知的信号通路协同刺激关节炎关节炎症过程中促炎介质的产生。脂联素在RA发病中的作用可能比以前认为的更重要。
To determine whether adiponectin may have synergistic effects in combination with the proinflammatory cytokine interleukin (IL)-1β regarding the production of proinflammatory mediators during arthritic joint inflammation, synovial cells from rheumatoid arthritis (RA) patients were treated with adiponectin, IL-1β, and their combination for 24 h. Culture supernatant was collected and analyzed by enzyme-linked immunosorbent assay for levels of IL-6, IL-8, prostaglandin E2 (PGE2), vascular endothelial growth factor (VEGF), and matrix metalloproteinases (MMPs). Adiponectin-mediated intracellular signaling pathways were investigated to elucidate the molecular mechanisms underlying their synergy. The association of proinflammatory mediators with adiponectin was investigated in the synovial fluid of arthritis patients. Adiponectin functioned synergistically with IL-1β to activate IL-6, IL-8, and PGE2 expression in RA fibroblast-like synoviocytes; Levels of VEGF, MMP-1, and MMP-13 were not synergistically stimulated. Adiponectin and IL-1β each increased the expression of both adiponectin receptor 1 and IL-1 receptor 1. However, adiponectin and IL-1β did not synergistically support the degradation of IκB-α or the nuclear translocation of NF-κB. Synergistically increased gene expression was significantly inhibited by MG132, an NF-κB inhibitor. Supporting the in vitro results, IL-6 and IL-8 levels were positively associated with adiponectin in synovial joint fluid from patients with RA, but not osteoarthritis (OA). In conclusion, adiponectin and IL-1β may synergistically stimulate the production of proinflammatory mediators through unknown signaling pathways during arthritic joint inflammation. Adiponectin may be more important to the pathogenesis of RA than previously thought.
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影响因子：
4.4
作者：
Ehling, Angela;Schaeffler, Andreas;Mueller-Ladner, Ulf
通讯作者：
Mueller-Ladner, Ulf
影响因子：
4
作者：
Choi, Hyun Mi;Oh, Da Hee;Kim, Kyoung Soo
通讯作者：
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影响因子：
82.9
作者：
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通讯作者：
Matsuzawa, Y
DOI：
10.1016/j.ecl.2008.07.002
发表时间：
2008-09
影响因子：
4.5
作者：
Halberg, Nils;Wernstedt-Asterholm, Ingrid;Scherer, Philipp E.
通讯作者：
Scherer, Philipp E.
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影响因子：
4.9
作者：
Kim, Kyoung Soo;Park, Eun Kyung;Ju, Seung Min;Jung, Hye-Sook;Bang, Jun Soo;Kim, Chaekyun;Lee, Yeon-Ah;Hong, Seung-Jae;Lee, Sang-Hoon;Yang, Hyung-In;Yoo, Myung Chul
通讯作者：
Yoo, Myung Chul