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Biol Pharm Bull ; 40(3): 352-356, 2017.
Article in English | MEDLINE | ID: mdl-28250278

ABSTRACT

Osteoclasts represent the only bone resorbing cells in an organism. In this study, we investigated the effect of glucosamine (GlcN), a nutrient used to prevent joint pain and bone loss, on the osteoclastogenesis of murine macrophage-like RAW264 cells. GlcN supplementation suppressed the upregulation of osteoclast-specific genes (tartrate-resistant acid phosphatase (TRAP), cathepsin K, matrix metallopeptidase 9, and nuclear factor of activated T cell c1 (NFATc1)), receptor activator of nuclear factor-κB ligand (RANKL)-dependent upregulation of TRAP enzyme activity, and the formation of TRAP-positive multinuclear cells more effectively than N-acetylglucosamine (GlcNAc), which we have previously shown to inhibit osteoclast differentiation. To clarify the mechanism by which GlcN suppresses osteoclastogenesis, we further investigated the effect of GlcN on O-GlcNAcylation by Western blotting and on other types of glycosylation by lectin blotting. We found that, upon addition of GlcN, the O-GlcNAcylation of cellular proteins was increased whereas α2,6-linked sialic acid modification was decreased. Therefore, these glycan modifications in cellular proteins may contribute to the suppression of osteoclastogenesis.


Subject(s)
Cell Differentiation/drug effects , Glucosamine/pharmacology , Osteoclasts/drug effects , Osteogenesis/drug effects , Protein Processing, Post-Translational/drug effects , Acylation , Animals , Bone Resorption/metabolism , Cell Line , Glycosylation , Macrophages/drug effects , Macrophages/metabolism , Mice , Osteoclasts/metabolism , RANK Ligand/metabolism , Tartrate-Resistant Acid Phosphatase/metabolism , Up-Regulation
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