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Effects of Inositol 1,4,5-triphosphate on Osteoclast Differentiation in RANKL-induced Osteoclastogenesis.
DC Field | Value | Language |
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dc.contributor.author | 손아란 | - |
dc.contributor.author | 신동민 | - |
dc.date.accessioned | 2014-12-19T17:23:53Z | - |
dc.date.available | 2014-12-19T17:23:53Z | - |
dc.date.issued | 2012 | - |
dc.identifier.issn | 1226-4512 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/91332 | - |
dc.description.abstract | The receptor activator of NF-κB ligand (RANKL) signal is an activator of tumor necrosis factor receptor-associated factor 6 (TRAF6), which leads to the activation of NF-κB and other signal transduction pathways essential for osteoclastogenesis, such as Ca(2+) signaling. However, the intracellular levels of inositol 1,4,5-trisphosphate (IP(3)) and IP(3)-mediated cellular function of RANKL during osteoclastogenesis are not known. In the present study, we determined the levels of IP(3) and evaluated IP(3)-mediated osteoclast differentiation and osteoclast activity by RANKL treatment of mouse leukemic macrophage cells (RAW 264.7) and mouse bone marrow-derived monocyte/macrophage precursor cells (BMMs). During osteoclastogenesis, the expression levels of Ca(2+) signaling proteins such as IP(3) receptors (IP(3)Rs), plasma membrane Ca(2+) ATPase, and sarco/endoplasmic reticulum Ca(2+) ATPase type2 did not change by RANKL treatment for up to 6 days in both cell types. At 24 h after RANKL treatment, a higher steady-state level of IP(3) was observed in RAW264.7 cells transfected with green fluorescent protein (GFP)-tagged pleckstrin homology (PH) domains of phospholipase C (PLC) δ, a probe specifically detecting intracellular IP(3) levels. In BMMs, the inhibition of PLC with U73122 [a specific inhibitor of phospholipase C (PLC)] and of IP(3)Rs with 2-aminoethoxydiphenyl borate (2APB; a non-specific inhibitor of IP(3)Rs) inhibited the generation of RANKL-induced multinucleated cells and decreased the bone-resorption rate in dentin slice, respectively. These results suggest that intracellular IP(3) levels and the IP(3)-mediated signaling pathway play an important role in RANKL-induced osteoclastogenesis. | - |
dc.description.statementOfResponsibility | open | - |
dc.relation.isPartOf | KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.title | Effects of Inositol 1,4,5-triphosphate on Osteoclast Differentiation in RANKL-induced Osteoclastogenesis. | - |
dc.type | Article | - |
dc.contributor.college | College of Dentistry (치과대학) | - |
dc.contributor.department | Dept. of Oral Biology (구강생물학) | - |
dc.contributor.googleauthor | Aran Son | - |
dc.contributor.googleauthor | Min Seuk Kim | - |
dc.contributor.googleauthor | Hae Jo | - |
dc.contributor.googleauthor | Hae Mi Byun | - |
dc.contributor.googleauthor | Dong Min Shin | - |
dc.identifier.doi | 22416217 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A01980 | - |
dc.contributor.localId | A02091 | - |
dc.relation.journalcode | J02104 | - |
dc.identifier.eissn | 2093-3827 | - |
dc.identifier.pmid | 22416217 | - |
dc.subject.keyword | Ca2+ signaling | - |
dc.subject.keyword | Inositol 1,4,5-trisphosphate | - |
dc.subject.keyword | Osteoclastogenesis | - |
dc.subject.keyword | RANKL | - |
dc.contributor.alternativeName | Son, Aran | - |
dc.contributor.alternativeName | Shin, Dong Min | - |
dc.contributor.affiliatedAuthor | Son, Aran | - |
dc.contributor.affiliatedAuthor | Shin, Dong Min | - |
dc.citation.volume | 16 | - |
dc.citation.number | 1 | - |
dc.citation.startPage | 31 | - |
dc.citation.endPage | 36 | - |
dc.identifier.bibliographicCitation | KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY, Vol.16(1) : 31-36, 2012 | - |
dc.identifier.rimsid | 30114 | - |
dc.type.rims | ART | - |
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