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C-C 趋化因子配体 19 和 21 对破骨细胞迁移和骨吸收的刺激作用。

Stimulation of osteoclast migration and bone resorption by C-C chemokine ligands 19 and 21.

机构信息

Department of Cell and Developmental Biology, BK21 Program and Dental Research Institute, Seoul National University, Seoul, Korea.

Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, and College of Medicine, Seoul National University, Seoul, Korea.

出版信息

Exp Mol Med. 2017 Jul 21;49(7):e358. doi: 10.1038/emm.2017.100.

DOI:10.1038/emm.2017.100
PMID:28729639
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5565950/
Abstract

Osteoclasts are responsible for the bone erosion associated with rheumatoid arthritis (RA). The upregulation of the chemokines CCL19 and CCL21 and their receptor CCR7 has been linked to RA pathogenesis. The purpose of this study was to evaluate the effects of CCL19 and CCL21 on osteoclasts and to reveal their underlying mechanisms. The expression of CCL19, CCL21 and CCR7 was higher in RA patients than in osteoarthritis patients. In differentiating osteoclasts, tumor necrosis factor-α, interleukin-1β and lipopolysaccharide stimulated CCR7 expression. CCL19 and CCL21 promoted osteoclast migration and resorption activity. These effects were dependent on the presence of CCR7 and abolished by the inhibition of the Rho signaling pathway. CCL19 and CCL21 promoted bone resorption by osteoclasts in an in vivo mice calvarial model. These findings demonstrate for the first time that CCL19, CCL21 and CCR7 play important roles in bone destruction by increasing osteoclast migration and resorption activity. This study also suggests that the interaction of CCL19 and CCL21 with CCR7 is an effective strategic focus in developing therapeutics for alleviating inflammatory bone destruction.

摘要

破骨细胞负责与类风湿关节炎（RA）相关的骨质侵蚀。趋化因子 CCL19 和 CCL21 及其受体 CCR7 的上调与 RA 的发病机制有关。本研究旨在评估 CCL19 和 CCL21 对破骨细胞的影响，并揭示其潜在机制。CCL19、CCL21 和 CCR7 在 RA 患者中的表达高于骨关节炎患者。在破骨细胞分化过程中，肿瘤坏死因子-α、白细胞介素-1β 和脂多糖刺激 CCR7 的表达。CCL19 和 CCL21 促进破骨细胞迁移和吸收活性。这些作用依赖于 CCR7 的存在，并被 Rho 信号通路的抑制所消除。CCL19 和 CCL21 在体内小鼠颅骨模型中促进破骨细胞的骨吸收。这些发现首次表明，CCL19、CCL21 和 CCR7 通过增加破骨细胞的迁移和吸收活性，在骨破坏中发挥重要作用。本研究还表明，CCL19 和 CCL21 与 CCR7 的相互作用是开发治疗炎症性骨破坏药物的有效策略重点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a706/5565950/c343aec6d3c2/emm2017100f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a706/5565950/fe7ddb4d00db/emm2017100f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a706/5565950/85cc598605bc/emm2017100f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a706/5565950/fb4df67c9aba/emm2017100f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a706/5565950/c532b39795cf/emm2017100f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a706/5565950/3a884eb1de8c/emm2017100f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a706/5565950/f649370cd508/emm2017100f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a706/5565950/2ba53edb828a/emm2017100f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a706/5565950/c343aec6d3c2/emm2017100f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a706/5565950/fe7ddb4d00db/emm2017100f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a706/5565950/85cc598605bc/emm2017100f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a706/5565950/fb4df67c9aba/emm2017100f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a706/5565950/c532b39795cf/emm2017100f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a706/5565950/3a884eb1de8c/emm2017100f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a706/5565950/f649370cd508/emm2017100f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a706/5565950/2ba53edb828a/emm2017100f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a706/5565950/c343aec6d3c2/emm2017100f8.jpg

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Stimulation of osteoclast migration and bone resorption by C-C chemokine ligands 19 and 21.

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本文引用的文献

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Epigenetic control of Ccr7 expression in distinct lineages of lung dendritic cells.

J Immunol. 2014-11-15

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Biochem Biophys Res Commun. 2014-7-30

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A myriad of functions and complex regulation of the CCR7/CCL19/CCL21 chemokine axis in the adaptive immune system.

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Osteoclast migration, differentiation and function: novel therapeutic targets for rheumatic diseases.

Rheumatology (Oxford). 2012-9-28

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