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麻疹病毒核衣壳蛋白是 Pagets 病的关键致病因子,通过下调 FoxO3/Sirt1 信号通路增加 IL-6 的表达。

Measles virus nucleocapsid protein, a key contributor to Paget's disease, increases IL-6 expression via down-regulation of FoxO3/Sirt1 signaling.

机构信息

Department of Medicine/Hematology-Oncology, University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, 5117 Centre Avenue, Research Pavilion, Room 1.19b, Pittsburgh, PA 15213, USA.

出版信息

Bone. 2013 Mar;53(1):269-76. doi: 10.1016/j.bone.2012.12.007. Epub 2012 Dec 20.

Abstract

Measles virus plays an important role as an environmental factor in the pathogenesis of Paget's disease (PD). Previous studies have shown that IL-6 is increased in the bone marrow of Paget's patients and that measles virus nucleocapsid protein (MVNP) induces IL-6 secretion by pagetic osteoclasts. Further, IL-6 plays a critical role in the development of pagetic osteoclasts and bone lesions induced by PD, but the mechanisms regulating IL-6 production by MVNP remain unclear. Our current studies revealed that MVNP expression in osteoclast precursors down-regulated Sirt1 mRNA and protein, a negative regulator of NF-κB activity, which is a key factor for IL-6 expression. MVNP expression in NIH3T3 cells also elevated Il-6 transcription and impaired the expression of Sirt1 mRNA both under basal conditions and upon activation of the Sirt1 upstream regulator FoxO3 by LY294002 (a PI3K/AKT inhibitor). Luciferase activity assays showed that constitutively active FoxO3 abolished the repressive effect of MVNP on reporters driven by either FoxO3 response elements or the Sirt1 promoter. Further, protein stability assays revealed that FoxO3 was degraded more rapidly in MVNP-expressing cells than in control cells following the addition of cycloheximide. Similarly, co-transfection of MVNP and FoxO3 into HEK293 cells demonstrated that MVNP decreased the protein levels of over-expressed FoxO3 in a dose-dependent manner. Treatment with the proteasome inhibitor, MG132, blocked the MVNP-triggered decrease of FoxO3, and the treatment with the serine/threonine phosphatase inhibitor, calyculin A, revealed that MVNP increased phosphorylation of FoxO3. Further, over-expression of Sirt1 or treatment with the Sirt1 activator resveratrol blocked the increase in Il-6 transcription by MVNP. Finally, resveratrol reduced the numbers of TRAP positive multi-nuclear cells in bone marrow cultures from TRAP-MVNP transgenic mice to wild type levels. These results indicate that MVNP decreases FoxO3/Sirt1 signaling to enhance the levels of IL-6, which in part mediate MVNP's contribution to the development of Paget's disease.

摘要

麻疹病毒在 Pagetic 病(PD)发病机制中作为环境因素起着重要作用。先前的研究表明,白细胞介素 6(IL-6)在 Pagetic 患者的骨髓中增加,麻疹病毒核衣壳蛋白(MVNP)诱导 Pagetic 破骨细胞分泌 IL-6。此外,IL-6 在 Pagetic 破骨细胞的发展和 PD 诱导的骨病变中起着关键作用,但调节 MVNP 产生 IL-6 的机制仍不清楚。我们目前的研究表明,MVNP 在破骨细胞前体中的表达下调了 Sirt1 mRNA 和蛋白,后者是 NF-κB 活性的负调节剂,是 IL-6 表达的关键因素。MVNP 在 NIH3T3 细胞中的表达也升高了 Il-6 转录,并损害了 Sirt1 mRNA 的表达,无论是在基础条件下还是在 LY294002(PI3K/AKT 抑制剂)激活 Sirt1 上游调节因子 FoxO3 的情况下。荧光素酶活性测定表明,组成型激活的 FoxO3 消除了 MVNP 对 FoxO3 反应元件或 Sirt1 启动子驱动的报告基因的抑制作用。此外,蛋白质稳定性测定表明,与对照细胞相比,MVNP 表达细胞中 FoxO3 在加入环己酰亚胺后更快降解。同样,将 MVNP 和 FoxO3 共转染到 HEK293 细胞中表明,MVNP 以剂量依赖的方式降低了过表达 FoxO3 的蛋白水平。用蛋白酶体抑制剂 MG132 处理可阻断 MVNP 触发的 FoxO3 减少,而用丝氨酸/苏氨酸磷酸酶抑制剂 calyculin A 处理表明 MVNP 增加了 FoxO3 的磷酸化。此外,Sirt1 的过表达或 Sirt1 激活剂白藜芦醇的处理阻断了 MVNP 对 Il-6 转录的增加。最后,白藜芦醇将 TRAP-MVNP 转基因小鼠骨髓培养物中 TRAP 阳性多核细胞的数量减少到野生型水平。这些结果表明,MVNP 降低了 FoxO3/Sirt1 信号转导,以增强 IL-6 的水平,这部分介导了 MVNP 对 Pagetic 病发展的贡献。

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