Osteoclast stimulatory transmembrane protein and dendritic cell–specific transmembrane protein cooperatively modulate cell–cell fusion to form osteoclasts and foreign body giant cells

Miyamoto, Hiroaki; Suzuki, Takayuki; Miyauchi, Yoshiteru; Iwasaki, Ryuichiro; Kobayashi, Tami; Sato, Yuiko; Miyamoto, Kana; Hoshi, Hiroko; Hashimoto, Kazuaki; Yoshida, Shigeyuki; Wu, Hao; Mori, Tomoaki; Kanagawa, Hiroya; Katsuyama, Eri; Fujie, Atsuhiro; Morioka, Hideo; Matsumoto, Morio; Chiba, Kazuhiro; Takeya, Motohiro; Toyama, Yoshiaki; Miyamoto, Takeshi

doi:10.1002/jbmr.1575

Cited by 144 publications

(146 citation statements)

References 33 publications

Supporting

Mentioning

130

Contrasting

Order By: Relevance

“…TRAP (48), cathepsin K (49), and MMP9 (50) are required for the bone resorptive activity of mature osteoclast, whereas osteoclast stimulatory transmembrane protein is essential for cell-cell fusion of osteoclasts (51). On the basis of promoter analyses, TRAP (30,52,53), cathepsin K (52, 54), and MMP9 (55) are regulated by NFATc1.…”

Section: Discussionmentioning

confidence: 99%

The Dectin 1 Agonist Curdlan Regulates Osteoclastogenesis by Inhibiting Nuclear Factor of Activated T cells Cytoplasmic 1 (NFATc1) through Syk Kinase

Yamasaki

Ariyoshi²,

Okinaga³

et al. 2014

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Dectin 1 is found on myeloid lineage cells and contains an immunoreceptor tyrosine-based activation motif from which signals are associated with bone homeostasis. Results: The dectin 1 agonist curdlan suppresses osteoclastogenesis induced by receptor activator of NF-B ligand (RANKL). Conclusion: Curdlan regulates RANKL-induced osteoclastogenesis.Significance: Curdlan could be a potential therapeutic candidate in treating osteoclast-related diseases.

show abstract

Section: Discussionmentioning

confidence: 99%

The Dectin 1 Agonist Curdlan Regulates Osteoclastogenesis by Inhibiting Nuclear Factor of Activated T cells Cytoplasmic 1 (NFATc1) through Syk Kinase

Yamasaki

Ariyoshi²,

Okinaga³

et al. 2014

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…It has been reported recently that Atp6v0d2 interacts with adhesion-regulating molecule 1 (ADAM1) protein and regulates osteoclast multinucleation (16) and that DC-STAMP cooperates with osteoclast stimulatory transmembrane protein (OC-STAMP) in promoting cell-cell fusion of preosteoclasts (63). In addition, Atp6v0d2 has been shown to possess the differentiation-specific dual functions as a regulator of cell-cell fusion at the early preosteoclast stage and as an essential component of the osteoclastspecific proton pump in bone resorption (17).…”

Section: Discussionmentioning

confidence: 99%

Low-density Lipoprotein Receptor Deficiency Causes Impaired Osteoclastogenesis and Increased Bone Mass in Mice because of Defect in Osteoclastic Cell-Cell Fusion

Okayasu

Nakayachi

Hayashida

et al. 2012

Journal of Biological Chemistry

View full text Add to dashboard Cite

“…DC-STAMP and OC-STAMP modulate cell-cell fusion in osteoclasts, and are induced by the RANKL-NFATc1 axis (37). Decreased expression of DC-STAMP and OC-STAMP inhibit the fusion of osteoclasts.…”

Section: A B C D E F H G Imentioning

confidence: 99%

Release from optimal compressive force suppresses osteoclast differentiation

Ikeda

Yoshimura

Kikuiri

et al. 2016

Molecular Medicine Reports

View full text Add to dashboard Cite

Abstract. Bone remodeling is an important factor in orthodontic tooth movement. During orthodontic treatment, osteoclasts are subjected to various mechanical stimuli, and this promotes or inhibits osteoclast differentiation and fusion. It has been previously reported that the release from tensile force induces osteoclast differentiation. However, little is known about how release from compressive force affects osteoclasts. The present study investigated the effects of release from compressive force on osteoclasts. The number of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated osteoclasts derived from RAW264.7 cells was counted, and gene expression associated with osteoclast differentiation and fusion in response to release from compressive force was evaluated by reverse transcription-quantitative polymerase chain reaction. Osteoclast number was increased by optimal compressive force application. On release from this force, osteoclast differentiation and fusion were suppressed. mRNA expression of NFATc1 was inhibited for 6 h subsequent to release from compressive force. mRNA expression of the other osteoclast-specific genes, TRAP, RANK, matrix metalloproteinase-9, cathepsin-K, chloride channel 7, ATPase H + transporting vacuolar proton pump member I, dendritic cell-specific transmembrane protein and osteoclast stimulatory transmembrane protein (OC-STAMP) was significantly inhibited at 3 h following release from compressive force compared with control cells. These findings suggest that release from optimal compressive force suppresses osteoclast differentiation and fusion, which may be important for developing orthodontic treatments.

show abstract

Osteoclast stimulatory transmembrane protein and dendritic cell–specific transmembrane protein cooperatively modulate cell–cell fusion to form osteoclasts and foreign body giant cells

Cited by 144 publications

References 33 publications

The Dectin 1 Agonist Curdlan Regulates Osteoclastogenesis by Inhibiting Nuclear Factor of Activated T cells Cytoplasmic 1 (NFATc1) through Syk Kinase

The Dectin 1 Agonist Curdlan Regulates Osteoclastogenesis by Inhibiting Nuclear Factor of Activated T cells Cytoplasmic 1 (NFATc1) through Syk Kinase

Low-density Lipoprotein Receptor Deficiency Causes Impaired Osteoclastogenesis and Increased Bone Mass in Mice because of Defect in Osteoclastic Cell-Cell Fusion

Release from optimal compressive force suppresses osteoclast differentiation

Contact Info

Product

Resources

About