Characterization of CCL19 and CCL21 in rheumatoid arthritis.
Characterization of CCL19 and CCL21 in rheumatoid arthritis.
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DOI：
10.1002/art.30232
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发表时间：
2011-04
影响因子：
--
通讯作者：
Shahrara, Shiva
中科院分区：
文献类型：
--
作者：
Pickens, Sarah R.;Chamberlain, Nathan D.;Volin, Michael V.;Pope, Richard M.;Mandelin, Arthur M., II;Shahrara, Shiva
目的是表征类风湿关节炎（RA）滑膜组织中CCL 19和CCL 21的表达，并检查它们在巨噬细胞和RA滑膜组织成纤维细胞中的调节和致病作用。采用免疫组化法检测了CCL 19和CCL 21在RA和正常滑膜组织中的表达。使用ELISA定量来自骨关节炎（OA）、幼年特发性关节炎（JIA）、银肩病关节炎（PsA）和RA的流体中的CCL 19和CCL 21水平。通过实时RT-PCR测定RA外周血中体外分化的巨噬细胞以及RA滑膜组织成纤维细胞中CCL 19和CCL 21表达的调节。采用ELISA检测CCL 19和CCL 21激活的外周血体外分化的巨噬细胞和RA滑膜组织成纤维细胞的促血管生成因子产生。与NL对照相比，RA滑膜组织中的CCL 19和CCL 21升高。与OA滑液相比，RA和PsA滑液中的CCL 19和CCL 21水平显著升高。在RA巨噬细胞和成纤维细胞中，CCL 19的表达在LPS、TNF-α和IL-1β刺激下增加。然而，RA成纤维细胞中的IL-1β以及RA巨噬细胞中的TNF-α和RA滑液可调节CCL 21的表达。CCL 19和CCL 21激活诱导RA滑膜组织成纤维细胞产生VEGF和Ang-1，并诱导巨噬细胞分泌IL-8和Ang-1。我们首次在RA成纤维细胞和RA外周血体外分化的巨噬细胞中鉴定了CCL 19和CCL 21的调节剂，并记录了CCL 19/21在RA血管生成中的新作用。
The aim was to characterize the expression of CCL19 and CCL21 in rheumatoid arthritis (RA) synovial tissue and to examine their regulation and pathogenic role in macrophages and RA synovial tissue fibroblasts. Expression of CCL19 and CCL21 was demonstrated in RA and normal (NL) synovial tissues employing immunohistochemistry. CCL19 and CCL21 levels were quantified in fluids from osteoarthritis (OA), juvenile idiopathic arthritis (JIA), psoriatic arthritis (PsA) and RA using ELISA. Regulation of CCL19 and CCL21 expression was determined in RA peripheral blood in vitro differentiated macrophages as well as RA synovial tissue fibroblasts by real-time RT-PCR. CCL19 and CCL21 activated peripheral blood in vitro differentiated macrophages and RA synovial tissue fibroblasts were examined for proangiogenic factor production employing ELISA. CCL19 and CCL21 were elevated in RA synovial tissue compared to NL controls. Levels of CCL19 and CCL21 were greatly increased in RA and PsA synovial fluid versus OA synovial fluid. In RA macrophages and fibroblasts, expression of CCL19 was increased by LPS, TNF-α and IL-1β stimulation. However, CCL21 expression was modulated by IL-1β in RA fibroblasts as well as TNF-α and RA synovial fluid in RA macrophages. CCL19 and CCL21 activation induced VEGF and Ang-1 production from RA synovial tissue fibroblasts and secretion of IL-8 and Ang-1 from macrophages. We identify, for the first time, regulators of CCL19 and CCL21 in RA fibroblasts and RA peripheral blood in vitro differentiated macrophages and we document a novel role of CCL19/21 in RA angiogenesis.
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影响因子：
4
作者：
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通讯作者：
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影响因子：
32.4
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作者：
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