Journal Article Cellular function of osteocytes in normal and αklotho-deficient mice

Amizuka, Norio  ,  Hasegawa, Tomoka  ,  Yamamoto, Tomomaya  ,  Mae, Takahito  ,  Zixuan, Qiu  ,  Abe, Miki  ,  Shen, Zhao  ,  Nagai, Tomoya  ,  Yokoyama, Ayako  ,  Naznin, Khadiza  ,  Haraguchi, Mai  ,  Yamamoto, Tsuneyuki  ,  Freitas, Paulo Henrique Luiz de  ,  Li, Minqi

38 ( Special issue )  , pp.56 - 62 , 2017-09 , 北海道歯学会
During the last decade, osteocyte-derived factors i.e., sclerostin, dentin matrix protein-1, fibroblast growth factor 23 (FGF23) that reduces serum phosphate concentration by mediating FGF receptor 1c/αklotho in the kidney, have been highlighted for osteocytes’ fine-turned regulation on bone remodeling and phosphate homeostasis. Osteocytes are interconnected through gap junctions between their cytoplasmic processes, and thereby, build upon the functional syncytia, referred to as the osteocytic lacunar-canalicular system (OLCS). Osteocytes appear to communicate surrounding osteocytes and osteoblasts by means of two possible pathways of molecular transport throughout the OLCS : One is a passageway of their cytoplasmic processes, and the other is a pericellular space in the osteocytic canaliculi. The regularly-oriented OLCS in mature compact bone appears to efficiently serve for molecular transport, mechanosensing and targeted bone remodeling that would erase microdamages in bone. In a disrupted signaling state of FGF23/αklotho, serum concentration of phosphate would be markedly-elevated. Despite highly-elevated serum phosphate, αklotho -deficient mice revealed defective mineralization in bone matrix. OLCS in αklotho -deficient mice were irregularly-distributed and the connectivity of cytoplasmic processes of osteocytes was very poor, so that osteocytes did not seem to form functional syncytia. Therefore, osteocytes’function cooperated with other bone cells, rather than serum concentration of calcium/phosphate, and this seems to play a central role in maintaining bone mineralization. In this review, the biological function of the regularly-arranged OLCS in a normal state will be introduced, as well as dysfunctional osteocytes in αklotho-deficient state, using animal models.

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