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WAIF1 Is a Cell-Surface CTHRC1 Binding Protein Coupling Bone Resorption and Formation.

Kazuhiko Matsuoka1, Yukihiro Kohara1, Yoshinori Naoe1

  • 1Department of Bone and Joint Disease, National Center for Geriatrics and Gerontology, Obu, Aichi, Japan.

Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research
|April 7, 2018
PubMed
Summary

Osteoclast protein CTHRC1 binds WAIF1 on stromal cells, activating a novel pathway that links bone resorption to formation. This discovery reveals a key mechanism in bone remodeling and mass regulation.

Keywords:
BONE REMODELINGOSTEOBLASTSOSTEOCLASTSSTROMAL CELLS

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Area of Science:

  • Bone Biology
  • Cell Signaling
  • Molecular Mechanisms

Background:

  • Osteoclast-derived CTHRC1 (collagen triple helix repeat containing 1) promotes osteoblast differentiation.
  • The precise molecular mechanisms underlying CTHRC1's function in bone remodeling are not fully understood.

Purpose of the Study:

  • To elucidate the mechanism by which CTHRC1 stimulates osteoblast differentiation.
  • To identify the cell-surface protein that interacts with CTHRC1.
  • To investigate the role of this interaction in bone remodeling.

Main Methods:

  • Identified CTHRC1-binding protein using co-immunoprecipitation and mass spectrometry.
  • Analyzed gene expression patterns of CTHRC1 and its binding partner (Tpbg).
  • Utilized cell culture models (marrow stromal cells) and in vivo mouse models with genetic deletions (osteoblast lineage-specific Tpbg deletion).
  • Assessed alkaline phosphatase activity, protein signaling pathways (PKCδ, MEK/ERK), Rankl expression, bone formation, and bone resorption.

Main Results:

  • Wnt-activated inhibitory factor 1 (WAIF1), also known as 5T4, was identified as a cell-surface protein that binds CTHRC1.
  • The gene encoding WAIF1, Trophoblast glycoprotein (Tpbg), is highly expressed in bone and brain, similar to Cthrc1.
  • Downregulation of Tpbg in marrow stromal cells impaired CTHRC1 binding and CTHRC1-stimulated osteoblast differentiation via the WAIF1/PKCδ/ERK pathway.
  • Osteoblast lineage-specific deletion of Tpbg led to reduced Rankl expression, impaired bone formation and resorption, and hindered bone mass recovery after resorption, mimicking osteoclast-specific Cthrc1 deficiency.

Conclusions:

  • CTHRC1 binding to WAIF1 on stromal cells activates the PKCδ-ERK signaling pathway, promoting osteoblast differentiation.
  • This interaction represents a novel molecular link between bone resorption and formation during bone remodeling.
  • The CTHRC1-WAIF1 axis plays a critical role in regulating bone mass and coupling bone resorption with formation.