Increased synovial expression of transforming growth factor (TGF)-beta receptor endoglin and TGF-beta 1 in rheumatoid arthritis: possible interactions in the pathogenesis of the disease.
Increased synovial expression of transforming growth factor (TGF)-beta receptor endoglin and TGF-beta 1 in rheumatoid arthritis: possible interactions in the pathogenesis of the disease.
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DOI：
10.1006/clin.1995.1114
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发表时间：
1995-08
期刊：
影响因子：
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通讯作者：
Z. Szekanecz;G. Haines;L. Harlow;M. Shah;T. Fong;R. Fu;Samuel J.-W. Lin;Ghazi M. Rayan;Alisa E. Koch
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文献类型：
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作者：
Z. Szekanecz;G. Haines;L. Harlow;M. Shah;T. Fong;R. Fu;Samuel J.-W. Lin;Ghazi M. Rayan;Alisa E. Koch
炎症细胞进入类风湿性关节炎（RA）滑膜组织（ST）在这种疾病的发病机制中起作用。转化生长因子β（TGF-β）可能在这一过程中发挥作用。我们已经调查了endoglin的分布，一个新描述的受体TGF-β 1和β 3，在RA相比，骨关节炎（OA）或正常的ST。免疫组织化学分析进行了使用抗TGF-β 1单克隆抗体（mAb）以及10单克隆抗体提出的各种表位endoglin。本研究对10名RA患者、10名OA患者和4名正常人的ST进行了研究。RA组TGF-β 1表达明显高于OA组和正常ST段衬里细胞、间质巨噬细胞和内皮细胞（P < 0.05）。所有抗endoglin单克隆抗体均与RA、OA和正常ST中的内皮细胞反应。然而，10种抗内皮糖蛋白mAb中的3种与RA的反应明显多于正常ST衬里细胞（P < 0.05），并且与OA和正常巨噬细胞（P < 0.05）相比，RA的反应也明显更多。滑膜衬里层和滑膜下巨噬细胞TGF-β 1与endoglin的反应性呈正相关（P < 0.05）。这些结果表明，与正常ST相比，RA中骨髓成分上的TGF-β 1和Endoglin（一种TGF-β 1和-β 3受体）的某些表位上调。Endoglin也存在于ST内皮细胞上，其表达也可能增加与正常ST衬里细胞相比，OA上的表达也可能增加。这些发现暗示内皮糖蛋白在类风湿关节炎的发病机制。
The ingress of inflammatory cells into the rheumatoid (RA) synovial tissue (ST) plays a role in the pathogenesis of this disease. Transforming growth factor beta (TGF-beta) may play a role in this process. We have investigated the distribution of endoglin, a newly described receptor for TGF-beta 1 and -beta 3, in RA compared to osteoarthritis (OA) or normal ST. Immunohistochemical analysis was carried out using an anti-TGF-beta 1 monoclonal antibody (mAb) as well as 10 mAbs raised against various epitopes of endoglin. This study was performed on ST from 10 patients with RA, 10 with OA, and 4 normal individuals. TGF-beta 1 expression was significantly up-regulated on RA compared to OA and normal ST lining cells, interstitial macrophages, and endothelial cells (P < 0.05). All anti-endoglin mAbs uniformly reacted with endothelial cells in RA, OA, and normal STs. However, 3 out of 10 anti-endoglin mAbs reacted with significantly more RA versus normal ST lining cells (P < 0.05), as well as RA compared to OA and normal macrophages (P < 0.05). There was a positive correlation between TGF-beta 1 and endoglin reactivity on the synovial lining layer and subsynovial macrophages (P < 0.05). These results indicate that TGF-beta 1 and certain epitopes of endoglin, a TGF-beta 1 and -beta 3 receptor, are up-regulated on myeloid elements in RA compared to normal ST. Endoglin is also present on ST endothelia, and its expression may also be increased on OA compared to normal ST lining cells. These findings implicate endoglin in the pathogenesis of RA.