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成骨细胞衍生的微泡:成骨细胞与破骨细胞之间通讯的新机制。

Osteoblast-derived microvesicles: A novel mechanism for communication between osteoblasts and osteoclasts.

作者信息

Deng Lili, Wang Yaping, Peng Ying, Wu Yu, Ding Yuedi, Jiang Yuhai, Shen Zhenhai, Fu Qiang

机构信息

Key Laboratory of Nuclear Medicine, Ministry of Health, Jiangsu Key Laboratory of Molecular Nuclear Medicine, Jiangsu Institute of Nuclear Medicine, Wuxi, Jiangsu, China.

Wuxi Second People's Hospital of Nanjing Medical University, Wuxi, Jiangsu, China.

出版信息

Bone. 2015 Oct;79:37-42. doi: 10.1016/j.bone.2015.05.022. Epub 2015 May 24.

Abstract

The maintenance of bone homeostasis is largely dependent upon cellular communication between osteoclasts and osteoblasts. Microvesicles (MVs) have received a good deal of attention and are increasingly considered as mediators of intercellular communication due to their capacity to merge with and transfer a repertoire of bioactive molecular content (cargo) to recipient cells, triggering a variety of biologic responses. Here, we demonstrated that MVs shed from osteoblasts contain RANKL protein and can transfer it to osteoclast precursors through receptor ligand (RANKL-RANK), leading to stimulation of RANKL-RANK signaling to facilitate osteoclast formation. Such MV-mediated intercellular communication between osteoblasts and osteoclasts may represent a novel mechanism of bone modeling and remodeling. It may be worthwhile to further explore MVs as tools to modify the biological responses of bone cells or develop an alternative drug to treat bone diseases.

摘要

骨稳态的维持很大程度上依赖于破骨细胞与成骨细胞之间的细胞通讯。微泡(MVs)已受到广泛关注,并且由于其能够与受体细胞融合并转移一系列生物活性分子内容物(货物),从而触发各种生物学反应,因此越来越被视为细胞间通讯的介质。在此,我们证明了成骨细胞释放的微泡含有RANKL蛋白,并可通过受体配体(RANKL-RANK)将其转移至破骨细胞前体,从而刺激RANKL-RANK信号传导以促进破骨细胞形成。这种成骨细胞与破骨细胞之间由微泡介导的细胞间通讯可能代表了一种新的骨塑形和重塑机制。进一步探索将微泡作为改变骨细胞生物学反应的工具或开发治疗骨疾病的替代药物可能是值得的。

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