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Updated: Nov 26, 2025
09:37
A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation
Published on: March 15, 2018
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Dectin-1-mediated suppression of RANKL-induced osteoclastogenesis by glucan from baker's yeast
Shiika Hara1,2, Yoshie Nagai-Yoshioka1, Ryota Yamasaki1
1Division of Infections and Molecular Biology, Department of Health Promotion, Kyushu Dental University, Fukuoka, Japan.
Journal of Cellular Physiology
|December 11, 2020
Summary
Baker
Area of Science:
- Immunology and Cell Biology
- Skeletal Biology and Bone Diseases
Background:
- Immunoreceptors on osteoclast precursors regulate bone resorption.
- Dectin-1, a beta-glucan receptor, is expressed on these cells.
Purpose of the Study:
- To investigate the effect of beta-glucan on osteoclastogenesis.
- To explore beta-glucan as a potential therapeutic for bone diseases.
Main Methods:
- Assessed beta-glucan's bioactivity on receptor activator of nuclear factor-kappa B ligand (RANKL)-induced osteoclastogenesis.
- Utilized mouse bone marrow cells and dectin-1-overexpressing RAW264.7 (d-RAW) cells.
- Analyzed key signaling pathways including nuclear factor of activated T cell c1, nuclear factor-kappa B, Syk protein, c-fos, and Blimp1.
Main Results:
- Baker's yeast beta-glucan inhibited RANKL-induced osteoclastogenesis in both cell types.
- Suppressed key osteoclast differentiation markers (TRAP, Oc-stamp) and signaling molecules (NFATc1, NF-κB, c-fos, Blimp1).
- Induced degradation of Syk protein, crucial for osteoclast formation.
Conclusions:
- Baker's yeast beta-glucan effectively suppresses osteoclast formation.
- Suggests potential application of beta-glucan in treating bone-related diseases.
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