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Osteocyte‐intrinsic mTORC1 signaling restrains trabecular bone accrual in mice
Author(s) -
Liu Qingbai,
Liu Cunchang,
Yang Yanjun,
Yang Huilin,
Chen Jianquan
Publication year - 2018
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27470
Subject(s) - osteocyte , mtorc1 , microbiology and biotechnology , neuroscience , chemistry , biology , signal transduction , osteoblast , pi3k/akt/mtor pathway , biochemistry , in vitro
Mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) signaling plays important physiological roles in bone homeostasis by regulating multiple steps of osteoblast differentiation as well as its activity. However, its potential role in osteocytes has not been explored. In this study, we deleted Raptor , a specific and essential component of mTORC1, in osteocytes using Dmp1‐Cre . Deletion of Raptor in osteocytes did not affect bone development and growth, but caused compartment‐specific effects on bone mass. Osteocyte‐specific deletion of Raptor had no obvious effect on cortical bone compartments, but led to increased trabecular bone mass. Mechanistically, Raptor deletion resulted in decreased bone resorption without altering bone formation activity. Thus, our study revealed an unexpected role of osteocyte‐intrinsic mTORC1 signaling in limiting trabecular bone mass, suggesting that osteocyte‐specific inhibition of mTORC1 may be used as a novel approach to treatment of osteoporosis.