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Effects of Inositol 1,4,5-triphosphate on Osteoclast Differentiation in RANKL-induced Osteoclastogenesis.

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dc.contributor.author손아란-
dc.contributor.author신동민-
dc.date.accessioned2014-12-19T17:23:53Z-
dc.date.available2014-12-19T17:23:53Z-
dc.date.issued2012-
dc.identifier.issn1226-4512-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/91332-
dc.description.abstractThe 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.statementOfResponsibilityopen-
dc.relation.isPartOfKOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleEffects of Inositol 1,4,5-triphosphate on Osteoclast Differentiation in RANKL-induced Osteoclastogenesis.-
dc.typeArticle-
dc.contributor.collegeCollege of Dentistry (치과대학)-
dc.contributor.departmentDept. of Oral Biology (구강생물학)-
dc.contributor.googleauthorAran Son-
dc.contributor.googleauthorMin Seuk Kim-
dc.contributor.googleauthorHae Jo-
dc.contributor.googleauthorHae Mi Byun-
dc.contributor.googleauthorDong Min Shin-
dc.identifier.doi22416217-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01980-
dc.contributor.localIdA02091-
dc.relation.journalcodeJ02104-
dc.identifier.eissn2093-3827-
dc.identifier.pmid22416217-
dc.subject.keywordCa2+ signaling-
dc.subject.keywordInositol 1,4,5-trisphosphate-
dc.subject.keywordOsteoclastogenesis-
dc.subject.keywordRANKL-
dc.contributor.alternativeNameSon, Aran-
dc.contributor.alternativeNameShin, Dong Min-
dc.contributor.affiliatedAuthorSon, Aran-
dc.contributor.affiliatedAuthorShin, Dong Min-
dc.citation.volume16-
dc.citation.number1-
dc.citation.startPage31-
dc.citation.endPage36-
dc.identifier.bibliographicCitationKOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY, Vol.16(1) : 31-36, 2012-
dc.identifier.rimsid30114-
dc.type.rimsART-
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers

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