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A Simple Pit Assay Protocol to Visualize and Quantify Osteoclastic Resorption In Vitro
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Published on: June 16, 2022

Novel osteoclast signaling mechanisms.

Masahiro Shinohara1, Hiroshi Takayanagi

  • 1Department of Cell Signaling, Graduate School, Tokyo Medical and Dental University and COE Program for Frontier Research on Molecular Destruction and Reconstruction of Tooth and Bone, Yushima 1-5-45, Bunkyo-ku, Tokyo 113-8549, Japan. taka.csi@tmd.ac.jp

Current Osteoporosis Reports
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Summary

Osteoclast differentiation relies on Receptor activator of NF-kappaB ligand (RANKL) signaling. Key pathways include NFATc1 activation and calcium signaling, crucial for bone resorption and osteoclastogenesis.

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Osteoclast Derivation from Mouse Bone Marrow
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06:17

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Published on: November 6, 2014

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Immunology

Background:

  • Osteoclasts, derived from monocytes/macrophages, are essential for bone matrix degradation.
  • Receptor activator of NF-kappaB ligand (RANKL) is a critical inducer of osteoclast differentiation.
  • Understanding osteoclast signaling is vital for bone metabolism research.

Purpose of the Study:

  • To review recent advances in the signaling mechanisms governing osteoclast differentiation.
  • To highlight the key molecular players and pathways involved in osteoclastogenesis.
  • To provide a comprehensive overview of osteoclast biology.

Main Methods:

  • Review of existing literature on osteoclast differentiation signaling.
  • Analysis of molecular pathways including RANKL, NFATc1, and calcium signaling.
  • Integration of findings on immunoreceptor tyrosine-based activation motif (ITAM) signaling.

Main Results:

  • RANKL activates multiple pathways, including tumor necrosis factor receptor-associated factor 6, c-Fos, and calcium signaling.
  • Nuclear factor of activated T cells (NFAT) c1 is identified as the master transcription factor for osteoclast differentiation.
  • Costimulatory signals via ITAM-associated receptors activate calcium signaling through phospholipase Cgamma (PLCgamma).
  • The CaMK-CREB pathway is also crucial for osteoclastogenesis, alongside calcineurin-NFATc1.

Conclusions:

  • Osteoclast differentiation is a complex process regulated by intricate signaling networks.
  • NFATc1 and calcium signaling pathways are indispensable for osteoclast formation and function.
  • Further research into these pathways can inform therapeutic strategies for bone diseases.