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F4/80 inhibits osteoclast differentiation via downregulation of nuclear factor of activated T cells, cytoplasmic 1

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dc.contributor.authorKang, Ju-Hee-
dc.contributor.authorSim, Jung-Sun-
dc.contributor.authorZheng, Ting-
dc.contributor.authorYim, Mijung-
dc.date.available2021-02-22T11:15:20Z-
dc.date.issued2017-04-
dc.identifier.issn0253-6269-
dc.identifier.issn1976-3786-
dc.identifier.urihttps://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/8584-
dc.description.abstractOsteoclastogenesis is an essential process in bone metabolism, which can be induced by RANKL stimulation. The F4/80 glycoprotein is a member of the EGF-transmembrane 7 (TM7) family and has been established as a specific cell-surface marker for murine macrophages. This study aimed to identify the role of F4/80 in osteoclastogenesis. Using mouse bone marrow-derived macrophages (BMMs), we observed that the mRNA level of F4/80 was dramatically reduced as these cells differentiated into osteoclasts. Furthermore, osteoclastogenesis was decreased in F4/80(high) BMMs compared to F4/80(-/low) BMMs. The inhibitory effect of F4/80 was associated with decreased expression of nuclear factor of activated T cells, cytoplasmic 1 (NFATc1). Ectopic overexpression of a constitutively active form of NFATc1 rescued the anti-osteoclastogenic effect of F4/80 completely, suggesting that the anti-osteoclastogenic effect of F4/80 was mainly due to reduction in NFATc1 expression. As an underlying mechanism, we demonstrated that the presence of F4/80 abrogated the effect of RANKL on the phosphorylation of CREB and activated the expression of IFN-beta, which are restored by cyclic AMP. Collectively, our results demonstrate that the presence of F4/80 suppresses RANKL-induced osteoclastogenesis by impairing the expression of NFATc1 via CREB and IFN-beta. Therefore, F4/80 may hold therapeutic potential for bone destructive diseases.-
dc.format.extent8-
dc.language영어-
dc.language.isoENG-
dc.publisherPHARMACEUTICAL SOC KOREA-
dc.titleF4/80 inhibits osteoclast differentiation via downregulation of nuclear factor of activated T cells, cytoplasmic 1-
dc.typeArticle-
dc.publisher.location대한민국-
dc.identifier.doi10.1007/s12272-017-0900-7-
dc.identifier.scopusid2-s2.0-85013104305-
dc.identifier.wosid000399161600008-
dc.identifier.bibliographicCitationARCHIVES OF PHARMACAL RESEARCH, v.40, no.4, pp 492 - 499-
dc.citation.titleARCHIVES OF PHARMACAL RESEARCH-
dc.citation.volume40-
dc.citation.number4-
dc.citation.startPage492-
dc.citation.endPage499-
dc.type.docTypeArticle-
dc.identifier.kciidART002215667-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
dc.relation.journalResearchAreaPharmacology & Pharmacy-
dc.relation.journalWebOfScienceCategoryChemistry, Medicinal-
dc.relation.journalWebOfScienceCategoryPharmacology & Pharmacy-
dc.subject.keywordPlusFACTOR-KAPPA-B-
dc.subject.keywordPlusRECEPTOR ACTIVATOR-
dc.subject.keywordPlusBONE-RESORPTION-
dc.subject.keywordPlusOSTEOPOROSIS-
dc.subject.keywordPlusINDUCTION-
dc.subject.keywordPlusLIGAND-
dc.subject.keywordPlusCREB-
dc.subject.keywordAuthorF4/80-
dc.subject.keywordAuthorOsteoclast-
dc.subject.keywordAuthorRANKL-
dc.subject.keywordAuthorNFATc1-
dc.subject.keywordAuthorBone loss-
dc.identifier.urlhttps://link.springer.com/article/10.1007%2Fs12272-017-0900-7-
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