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WNT16 Requires Gα Subunits as Intracellular Partners for Both Its Canonical and Non-Canonical WNT Signalling Activity

Gretl Hendrickx1,2, Eveline Boudin1, Marinus Verbeek1

  • 1Department of Medical Genetics, University of Antwerp, Antwerp, Belgium.

Calcified Tissue International
|November 25, 2019
PubMed

Insights

WNT16 enhances bone mass and strength by activating multiple WNT signaling pathways in osteoblasts. Specific Gα subunits are involved in WNT16

Area of Science:

  • Skeletal Biology and Bone Metabolism
  • Molecular Signaling Pathways
  • Cellular Biology

Background:

  • WNT16 is a key regulator of cortical bone, increasing bone mass and strength.
  • The precise WNT signaling mechanisms underlying WNT16's effects are not fully understood.
  • Canonical (WNT/β-catenin) and non-canonical (WNT/calcium, WNT/PCP) pathways are implicated in WNT signaling.

Purpose of the Study:

  • To investigate the modulation of canonical and non-canonical WNT signaling pathways by WNT16.
  • To elucidate the role of Gα subunits in WNT16-mediated signaling in osteoblasts.

Main Methods:

  • Investigated WNT/β-catenin, WNT/calcium, and WNT/PCP signaling in HEK293T and SaOS2 cells.
  • Performed knockdown of Gα12, Gα13, and Gαq subunits in osteoblasts.

Main Results:

  • WNT16 activated all WNT signaling pathways in osteoblasts.
  • WNT16 activated only WNT/calcium signaling in HEK293T cells.
  • Gα12, Gα13, and Gαq subunits are potentially involved in WNT16's WNT/β-catenin and WNT/calcium signaling, with Gα12 also implicated in WNT/PCP signaling.

Conclusions:

  • Defined WNT16's mechanism of action in osteoblasts, highlighting the interplay between WNT signaling pathways.
  • Identified a potential role for specific Gα subunits in WNT16 signaling.
  • Findings may inform future therapeutic strategies for skeletal homeostasis and fragility fractures.
Keywords:
Gα subunitsOsteoblastsWNT signallingWnt16

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