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Gα12 regulates osteoclastogenesis by modulating NFATc1 expression.

Min-Kyoung Song1, Cheolkyu Park1, Yong Deok Lee1

  • 1Department of Cell and Developmental Biology, BK21 Program and Dental Research Institute, Seoul National University, Seoul, Korea.

Journal of Cellular and Molecular Medicine
|October 28, 2017
PubMed
Summary

G protein Gα12 deficiency in mice leads to osteopetrosis, characterized by fewer osteoclasts and reduced bone resorption. Gα12 regulates osteoclast differentiation via NFATc1 and migration/resorption via RhoA signaling.

Keywords:
G alpha 12RhoAnuclear factor of activated T-cell c1osteoclastreceptor activator of nuclear factor κB ligand

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Area of Science:

  • Bone Biology
  • Cell Signaling
  • G Protein-Coupled Receptors

Background:

  • The G12 family of G protein alpha subunits regulates physiological processes.
  • The specific role of Gα12 in bone physiology remains largely undefined.

Purpose of the Study:

  • To investigate the function of Gα12 in bone metabolism and osteoclast biology.

Main Methods:

  • Micro-CT analysis of Gα12-knockout mice.
  • Histological examination of femoral tissue.
  • In vitro osteoclast differentiation assays using receptor activator of nuclear factor-κB ligand (RANKL).

Main Results:

  • Gα12-knockout mice exhibited an osteopetrotic phenotype with reduced osteoclast numbers.
  • Gα12 deficiency impaired osteoclast differentiation, decreased bone resorption activity, and suppressed RANKL-induced NFATc1 induction and RhoA activation.
  • NFATc1 induction by RANKL was independent of RhoA, but osteoclast migration and resorption required RhoA for Gα12-mediated regulation.

Conclusions:

  • Gα12 is crucial for osteoclastogenesis, regulating differentiation through NFATc1 and cell migration/resorption through RhoA signaling.