Osteocyte‐intrinsic mTORC1 signaling restrains trabecular bone accrual in mice. Issue 11 (30th August 2018)

• Record Type: Journal Article
• Authors: Liu, Qingbai; Liu, Cunchang; Yang, Yanjun; Yang, Huilin; Chen, Jianquan
• Is Part Of: Journal of cellular biochemistry. Volume 119:Issue 11(2018)
• Page Start: 8743
• Page End: 8749
• Publication Date: 2018-08-30
• Subjects: bone resorption -- mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) -- osteocytes -- raptor -- trabecular bone; Cytochemistry -- Periodicals; 572
• DOI: 10.1002/jcb.27470
• Languages: English
• ISSNs: 0730-2312

Abstract

Abstract: 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. Abstract : Deletion of Raptor in osteocytes led to increased trabecular bone mass likely due to diminished bone resorption. Thus, our study identified an unexpected role of osteocyte‐intrinsic mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) signaling in restraining trabecular bone accrual in mice.