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本文引用的文献

1
In vivo inhibition of angiogenesis by interleukin-13 gene therapy in a rat model of rheumatoid arthritis.白细胞介素-13基因治疗对类风湿性关节炎大鼠模型血管生成的体内抑制作用
Arthritis Rheum. 2007 Aug;56(8):2535-48. doi: 10.1002/art.22823.
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Constitutive upregulation of the transforming growth factor-beta pathway in rheumatoid arthritis synovial fibroblasts.类风湿性关节炎滑膜成纤维细胞中转化生长因子-β 通路的组成性上调。
Arthritis Res Ther. 2007;9(3):R59. doi: 10.1186/ar2217.
3
Chemokine and chemokine receptor analysis reveals elevated interferon-inducible protein-10 (IP)-10/CXCL10 levels and increased number of CCR5+ and CXCR3+ CD4 T cells in synovial fluid of patients with enthesitis-related arthritis (ERA).趋化因子及趋化因子受体分析显示,附着点炎相关关节炎(ERA)患者滑液中干扰素诱导蛋白-10(IP)-10/CXCL10水平升高,CCR5+和CXCR3+ CD4 T细胞数量增加。
Clin Exp Immunol. 2007 Jun;148(3):515-9. doi: 10.1111/j.1365-2249.2007.03377.x. Epub 2007 Mar 21.
4
Amelioration of inflammation, angiogenesis and CTGF expression in an arthritis model by a TSP1-derived peptide treatment.通过TSP1衍生肽治疗改善关节炎模型中的炎症、血管生成和CTGF表达。
J Cell Physiol. 2007 May;211(2):504-12. doi: 10.1002/jcp.20958.
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Blood and synovial fluid cytokine signatures in patients with juvenile idiopathic arthritis: a cross-sectional study.青少年特发性关节炎患者血液和滑液细胞因子特征:一项横断面研究。
Ann Rheum Dis. 2007 May;66(5):589-98. doi: 10.1136/ard.2006.061853. Epub 2006 Dec 14.
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A peptide from thrombospondin 1 modulates experimental erosive arthritis by regulating connective tissue growth factor.来自血小板反应蛋白1的一种肽通过调节结缔组织生长因子来调控实验性侵蚀性关节炎。
Arthritis Rheum. 2006 Aug;54(8):2415-22. doi: 10.1002/art.22021.
7
Increased expression of pro-inflammatory cytokines and metalloproteinase-1 by TGF-beta1 in synovial fibroblasts from rheumatoid arthritis and normal individuals.转化生长因子-β1在类风湿关节炎患者和正常个体的滑膜成纤维细胞中增加促炎细胞因子和金属蛋白酶-1的表达。
Clin Exp Immunol. 2002 Mar;127(3):547-52. doi: 10.1046/j.1365-2249.2002.01785.x.
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Multiplexed protein profiling on microarrays by rolling-circle amplification.通过滚环扩增在微阵列上进行多重蛋白质分析。
Nat Biotechnol. 2002 Apr;20(4):359-65. doi: 10.1038/nbt0402-359.
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Oxidized LDL-induced NF-kappa B activation and subsequent expression of proinflammatory genes are defective in monocyte-derived macrophages from CD36-deficient patients.氧化型低密度脂蛋白诱导的核因子κB激活以及随后促炎基因的表达在CD36缺陷患者的单核细胞衍生巨噬细胞中存在缺陷。
Arterioscler Thromb Vasc Biol. 2000 Aug;20(8):1953-60. doi: 10.1161/01.atv.20.8.1953.
10
Identification of known and novel genes in activated monocytes from patients with rheumatoid arthritis.类风湿性关节炎患者活化单核细胞中已知基因和新基因的鉴定。
Arthritis Rheum. 2000 Apr;43(4):775-90. doi: 10.1002/1529-0131(200004)43:4<775::AID-ANR8>3.0.CO;2-7.

血小板反应蛋白-1和转化生长因子β是类风湿性关节炎中的促炎分子。

Thrombospondin-1 and transforming growth factor beta are pro-inflammatory molecules in rheumatoid arthritis.

作者信息

Rico Mario C, Manns Joanne M, Driban Jeffrey B, Uknis Audrey B, Kunapuli Satya P, Dela Cadena Raul A

机构信息

Department of Physiology, The Sol Sherry Thrombosis Research Center, Temple University, Philadelphia, PA 19140, USA.

出版信息

Transl Res. 2008 Aug;152(2):95-8. doi: 10.1016/j.trsl.2008.06.002. Epub 2008 Jul 11.

DOI:10.1016/j.trsl.2008.06.002
PMID:18674744
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2529228/
Abstract

Thrombospondin-1 (TSP1/THBS1) plays a major role in the pathophysiology of rheumatoid arthritis (RA); however, its interface with the cytokine network involved in RA has not been delineated. Correlations were performed between plasma levels of TSP1 and selected cytokines from blood samples collected from 20 patients affected by RA and 13 healthy donors (control). Plasma levels of TSP1 and tissue growth factor beta (TGFbeta) were determined by standard enzyme-linked immunosorbent assay, and cytokines were measured by protein profiling rolling-circle amplification (RCA). TSP1 circulating levels in plasma were found significantly increased in the RA patients when compared with control individuals (P = 0.039). The plasma levels of TGFbeta were also increased in the RA patients, which indicates a statistical trend. Cytokine levels of interleukin (IL)-4, IL-5, IL-12, chemokine CXC 10 (CXCL10/IP10), and chemokine CC 4 (CCL4)/MIP1beta were significantly increased in the RA patients when compared with the control group. In summary, this study demonstrates increased plasma levels of TSP1, which correlated with increased levels of proinflammatory cytokines in plasma of RA patients. More detailed research is required to explore the cytokine imprint yielded by this study and its interface with TSP1 and TGFbeta.

摘要

血小板反应蛋白-1(TSP1/THBS1)在类风湿性关节炎(RA)的病理生理学中起主要作用;然而,其与RA中涉及的细胞因子网络的相互作用尚未明确。对20例RA患者和13名健康供体(对照)采集的血样中TSP1的血浆水平与选定的细胞因子进行了相关性分析。通过标准酶联免疫吸附测定法测定TSP1和组织生长因子β(TGFβ)的血浆水平,通过蛋白质谱滚环扩增(RCA)测量细胞因子。与对照个体相比,RA患者血浆中TSP1的循环水平显著升高(P = 0.039)。RA患者的血浆TGFβ水平也有所升高,这显示出一种统计学趋势。与对照组相比,RA患者的白细胞介素(IL)-4、IL-5、IL-12、趋化因子CXC 10(CXCL10/IP1)和趋化因子CC 4(CCL4)/MIP1β的细胞因子水平显著升高。总之,本研究表明RA患者血浆中TSP1水平升高,这与RA患者血浆中促炎细胞因子水平升高相关。需要更详细的研究来探索本研究产生的细胞因子印记及其与TSP1和TGFβ的相互作用。