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Osteocyte-intrinsic mTORC1 signaling restrains trabecular bone accrual in mice

Qingbai Liu1,2, Cunchang Liu3, Yanjun Yang3

  • 1Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Suzhou, China.

Journal of Cellular Biochemistry
|August 31, 2018
PubMed

Insights

Osteocyte-specific deletion of Raptor (a key mTORC1 component) increased trabecular bone mass by reducing bone resorption. This suggests inhibiting mTORC1 in osteocytes may treat osteoporosis.

Area of Science:

  • Bone Biology and Metabolism
  • Cellular Signaling Pathways

Background:

  • Mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) signaling is crucial for bone homeostasis.
  • Its role in osteocytes, critical bone cells, remains largely unexplored.

Purpose of the Study:

  • To investigate the function of osteocyte-intrinsic mTORC1 signaling in bone regulation.
  • To determine the effects of deleting Raptor, an essential mTORC1 component, specifically in osteocytes.

Main Methods:

  • Utilized Dmp1-Cre transgenic mice for osteocyte-specific deletion of the Raptor gene.
  • Analyzed bone development, growth, and mass using micro-computed tomography (micro-CT) and histomorphometry.
  • Assessed bone formation and resorption markers.

Main Results:

  • Osteocyte-specific Raptor deletion did not impact overall bone development or cortical bone mass.
  • Led to a significant increase in trabecular bone mass.
  • Mechanistically, this was attributed to decreased bone resorption without changes in bone formation.

Conclusions:

  • Osteocyte-intrinsic mTORC1 signaling plays an unexpected role in limiting trabecular bone mass.
  • Targeting osteocyte mTORC1 signaling represents a potential novel therapeutic strategy for osteoporosis.
Keywords:
bone resorptionmechanistic target of rapamycin (mTOR) complex 1 (mTORC1)osteocytesraptortrabecular bone

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