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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >The cation channel Trpv2 is a new suppressor of arthritis severity, joint damage, and synovial fibroblast invasion
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The cation channel Trpv2 is a new suppressor of arthritis severity, joint damage, and synovial fibroblast invasion

机译：阳离子通道Trpv2是关节炎严重程度，关节损伤和滑膜成纤维细胞浸润的新抑制剂

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摘要

Little is known about the regulation of arthritis severity and joint damage in rheumatoid arthritis (RA). Fibroblast-like synoviocytes (FLS) have a central role in joint damage and express increased levels of the cation channel Trpv2. We aimed at determining the role of Trpv2 in arthritis. Treatment with Trpv2-specific agonists decreased the in vitro invasiveness of FLS from RA patients and arthritic rats and mice. Trpv2 stimulation suppressed IL-1 beta-induced expression of MMP-2 and MMP-3. Trpv2 agonists, including the new and more potent LER13, significantly reduced disease severity in KRN serum- and collagen-induced arthritis, and reduced histologic joint damage, synovial inflammation, and synovial blood vessel numbers suggesting anti-angiogenic activity. In this first in vivo use of Trpv2 agonists we discovered a new central role for Trpv2 in arthritis. These new compounds have the potential to become new therapies for RA and other diseases associated with inflammation, invasion, and angiogenesis. (C) 2015 Elsevier Inc. All rights reserved.
机译：关于风湿性关节炎（RA）中关节炎严重程度和关节损伤的调节知之甚少。成纤维样滑膜细胞（FLS）在关节损伤中起关键作用，并表达增加水平的阳离子通道Trpv2。我们旨在确定Trpv2在关节炎中的作用。 Trpv2特异性激动剂的治疗降低了RA患者以及关节炎大鼠和关节炎小鼠FLS的体外侵袭性。 Trpv2刺激抑制IL-1β诱导的MMP-2和MMP-3表达。 Trpv2激动剂，包括新的和更有效的LER13，可显着降低KRN血清和胶原诱导的关节炎的疾病严重程度，并减少组织学关节损伤，滑膜炎症和滑膜血管数量，从而表明具有抗血管生成活性。在Trpv2激动剂的首次体内使用中，我们发现了Trpv2在关节炎中的新核心作用。这些新化合物有可能成为RA和与炎症，侵袭和血管生成有关的其他疾病的新疗法。 （C）2015 Elsevier Inc.保留所有权利。

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