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A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation
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WNT7B promotes bone formation in part through mTORC1.

Jianquan Chen1, Xiaolin Tu2, Emel Esen3

  • 1Department of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, Missouri, United States of America.

Plos Genetics
|February 6, 2014
PubMed
Summary

WNT7B significantly boosts bone formation by increasing osteoblast activity, acting through mTORC1 signaling. This WNT ligand enhances bone mass from embryonic development through adulthood.

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Area of Science:

  • Bone biology
  • Developmental biology
  • Molecular signaling

Background:

  • WNT signaling pathways are crucial for embryonic and postnatal bone development.
  • Specific WNT ligands and their downstream effects on osteogenesis remain incompletely understood.

Purpose of the Study:

  • To investigate the osteogenic potential of WNT7B and WNT5A in bone formation.
  • To elucidate the downstream signaling mechanisms by which WNT7B influences bone mass.

Main Methods:

  • Engineered mouse models for Cre-dependent expression of WNT7B and WNT5A in osteoblast lineages.
  • Utilized Runx2-lineage specific induction for postnatal WNT7B studies.
  • Assessed bone mass, osteoblast number, and activity.
  • Investigated the role of mTORC1 signaling via Raptor deletion.

Main Results:

  • Targeted WNT7B induction, but not WNT5A, dramatically increased bone mass.
  • WNT7B enhanced osteoblast number and activity, with effects observed from embryonic stages and intensifying postnatally.
  • WNT7B activated mTORC1 signaling through the PI3K-AKT pathway.
  • Disruption of mTORC1 signaling ameliorated the WNT7B-induced high-bone-mass phenotype.

Conclusions:

  • WNT7B is a potent stimulator of bone formation.
  • WNT7B promotes osteogenesis, at least in part, by activating mTORC1 signaling within the osteoblast lineage.