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Inhibition of Osteoclastogenesis by the RNA-Binding Protein QKI5: a Novel Approach to Protect from Bone Resorption.
Journal of Bone and Mineral Research ( IF 6.2 ) Pub Date : 2019-12-31 , DOI: 10.1002/jbmr.3943
Benjamin Rauwel 1 , Yannick Degboé 1, 2, 3 , Katy Diallo 1 , Souraya Sayegh 1 , Michel Baron 1 , Jean-Frédéric Boyer 1, 2 , Arnaud Constantin 1, 2, 3 , Alain Cantagrel 1, 2, 3 , Jean-Luc Davignon 1, 2
Affiliation  

Increased osteoclastogenesis is a common feature of bone erosion, notably in osteoporosis but also in inflammatory diseases such as rheumatoid arthritis (RA) and osteoarticular infections. Human cytomegalovirus (HCMV) infection has been described to impair monocyte differentiation into macrophages and dendritic cells. However, its effect on monocyte-derived osteoclasts is yet to be determined. We showed here that in vitro HCMV infection is associated with an inhibition of osteoclastogenesis through decreased expression of colony stimulating factor 1 receptor (CSF-1R) and RANK in monocytes, which was mediated by an upregulation of quaking I-5 protein (QKI-5), a cellular RNA-interacting protein. We found that deliberate QKI5 overexpression in the absence of HCMV infection is able to decrease CSF-1R and RANK expression, leading to osteoclastogenesis inhibition. Finally, by using lentiviral vectors in a calvarial bone erosion mouse model, we showed that QKI5 inhibits bone degradation. This work identifies QKI5 as a strong inhibitor of bone resorption. Future research will point out whether QKI5 could be a target for bone pathologies. © 2019 American Society for Bone and Mineral Research.

中文翻译:

RNA结合蛋白QKI5抑制破骨细胞生成:一种防止骨吸收的新方法。

破骨细胞生成增加是骨侵蚀的一个共同特征,特别是在骨质疏松症中,而且在类风湿性关节炎 (RA) 和骨关节感染等炎症性疾病中。人类巨细胞病毒 (HCMV) 感染已被描述为损害单核细胞向巨噬细胞和树突状细胞的分化。然而,其对单核细胞衍生的破骨细胞的影响尚待确定。我们在此表明​​,体外 HCMV 感染与通过降低单核细胞中集落刺激因子 1 受体 (CSF-1R) 和 RANK 的表达来抑制破骨细胞生成有关,这是由 quaking I-5 蛋白 (QKI-5) 的上调介导的。 ),一种细胞 RNA 相互作用蛋白。我们发现在没有 HCMV 感染的情况下故意 QKI5 过表达能够降低 CSF-1R 和 RANK 表达,导致破骨细胞生成抑制。最后,通过在颅骨侵蚀小鼠模型中使用慢病毒载体,我们发现 QKI5 抑制骨降解。这项工作将 QKI5 确定为骨吸收的强抑制剂。未来的研究将指出 QKI5 是否可以成为骨病变的靶点。© 2019 美国骨与矿物研究学会。
更新日期:2019-12-31
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