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

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 wit...

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Bibliographic Details
Published in:Bone (New York, N.Y.) N.Y.), 2015-10, Vol.79, p.37-42
Main Authors: Deng, Lili, Wang, Yaping, Peng, Ying, Wu, Yu, Ding, Yuedi, Jiang, Yuhai, Shen, Zhenhai, Fu, Qiang
Format: Article
Language:English
Subjects:
Animals
Blotting, Western
Bone Remodeling - physiology
Cell Communication - physiology
Cell Line
Cell-Derived Microparticles - metabolism
Cellular communication
Flow Cytometry
Mice
Microscopy, Confocal
Microscopy, Electron, Transmission
Microvesicles
Orthopedics
Osteoblast
Osteoblasts - metabolism
Osteoclast
Osteoclasts - metabolism
RANK Ligand - metabolism
RANKL–RANK pathway
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Summary: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.
ISSN:8756-3282
1873-2763
DOI:10.1016/j.bone.2015.05.022