Agelasine D suppresses RANKL-induced osteoclastogenesis via down-regulation of c-Fos, NFATc1 and NF-kB

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dc.contributor.authorMoo Rim Kang-
dc.contributor.authorSun Ah Jo-
dc.contributor.authorYeo Dae Yoon-
dc.contributor.authorKi Hwan Park-
dc.contributor.authorSoo Jin Oh-
dc.contributor.authorJi Eun Yun-
dc.contributor.authorChang Woo Lee-
dc.contributor.authorKi Hoan Nam-
dc.contributor.authorY Kim-
dc.contributor.authorS B Han-
dc.contributor.authorJ Yu-
dc.contributor.authorJ Rho-
dc.contributor.authorJong Soon Kang-
dc.date.accessioned2017-04-19T09:58:54Z-
dc.date.available2017-04-19T09:58:54Z-
dc.date.issued2014-
dc.identifier.issn1660-3397-
dc.identifier.uri10.3390/md12115643ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/12300-
dc.description.abstractIn the present study, we investigated the effect of agelasine D (AD) on osteoclastogenesis. Treatment of bone marrow macrophages (BMMs) with receptor activator of nuclear factor KB ligand (RANKL) resulted in a differentiation of BMMs into osteoclasts as evidenced by generation of tartrate-resistant acid phosphatase (TRAP)-positive, multinucleated cells and formation of pits in calcium phosphate-coated plates. However, RANKL-induced osteoclastogenesis was significantly suppressed by AD treatment. We also confirmed the increased mRNA and protein expression of osteoclastic markers, such as TRAP, cathepsin K and matrix metalloproteinase-9, during RANKL-induced osteoclast differentiation and this was down-regulated by AD treatment. Moreover, AD treatment significantly suppressed RANKL-induced mRNA expression of DC-STAMP and OC-STAMP and cell fusion of TRAP-positive mononuclear osteoclast precursors. In addition, AD suppressed RANKL-induced expression of transcription factors, c-Fos and nuclear factor of activated T cells c1 (NFATc1), which are important transcription factors involved in differentiation of BMMs into osteoclasts. Furthermore, RANKL-induced phosphorylation of extracellular signal-related kinase (ERK) and activation of NF-κB were also inhibited by AD treatment. Collectively, these results suggest that AD inhibits RANKL-induced osteoclastogenesis by down-regulation of multiple signaling pathways involving c-Fos, NFATc1, NF-κB and ERK. Our results also suggest that AD might be a potential therapeutic agent for prevention and treatment of osteoporosis.-
dc.publisherMDPI-
dc.titleAgelasine D suppresses RANKL-induced osteoclastogenesis via down-regulation of c-Fos, NFATc1 and NF-kB-
dc.title.alternativeAgelasine D suppresses RANKL-induced osteoclastogenesis via down-regulation of c-Fos, NFATc1 and NF-kB-
dc.typeArticle-
dc.citation.titleMarine Drugs-
dc.citation.number11-
dc.citation.endPage5656-
dc.citation.startPage5643-
dc.citation.volume12-
dc.contributor.affiliatedAuthorMoo Rim Kang-
dc.contributor.affiliatedAuthorSun Ah Jo-
dc.contributor.affiliatedAuthorYeo Dae Yoon-
dc.contributor.affiliatedAuthorKi Hwan Park-
dc.contributor.affiliatedAuthorSoo Jin Oh-
dc.contributor.affiliatedAuthorJi Eun Yun-
dc.contributor.affiliatedAuthorChang Woo Lee-
dc.contributor.affiliatedAuthorKi Hoan Nam-
dc.contributor.affiliatedAuthorJong Soon Kang-
dc.contributor.alternativeName강무림-
dc.contributor.alternativeName조선아-
dc.contributor.alternativeName윤여대-
dc.contributor.alternativeName박기환-
dc.contributor.alternativeName오수진-
dc.contributor.alternativeName윤지은-
dc.contributor.alternativeName이창우-
dc.contributor.alternativeName남기환-
dc.contributor.alternativeName김영수-
dc.contributor.alternativeName한상배-
dc.contributor.alternativeName유지연-
dc.contributor.alternativeName노재랑-
dc.contributor.alternativeName강종순-
dc.identifier.bibliographicCitationMarine Drugs, vol. 12, no. 11, pp. 5643-5656-
dc.identifier.doi10.3390/md12115643-
dc.subject.keywordAgelasine D-
dc.subject.keywordC-Fos-
dc.subject.keywordNF-ATc1-
dc.subject.keywordNF-κB-
dc.subject.keywordOsteoclastogenesis-
dc.subject.localAgelasine D-
dc.subject.localC-Fos-
dc.subject.localc-Fos-
dc.subject.localNF-ATc1-
dc.subject.localNFATc1-
dc.subject.localNuclear factor-kappa B-
dc.subject.localnuclear factor κB-
dc.subject.localNf-κb-
dc.subject.localNF-kB-
dc.subject.localnuclear factor kappa B-
dc.subject.localNF-κB (nuclear factor kappa-B)-
dc.subject.localNF-kappaB-
dc.subject.localNuclear factor-κb-
dc.subject.localNF-κ B-
dc.subject.localNF-κB-
dc.subject.localNF-kappa B-
dc.subject.localNuclear factor κB (NF-κB)-
dc.subject.localNuclear factor κB-
dc.subject.localNFκB-
dc.subject.localNf-κB-
dc.subject.localNuclear factor-κB-
dc.subject.localnuclear factorκB-
dc.subject.localNuclear factor (NF)-κB-
dc.subject.localNuclear factor kappa B-
dc.subject.localnuclear factor-κB-
dc.subject.localNF-ΚB-
dc.subject.localNuclear factor-kappa B (NF-κB)-
dc.subject.localNuclear factor-kappaB-
dc.subject.localnuclear factor-kappaB-
dc.subject.localnuclear factor-kappaB (NF-κB)-
dc.subject.localNFkappaB-
dc.subject.localNuclear factor kappaB-
dc.subject.localOsteoclastogenesis-
dc.subject.localosteoclastogenesis-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > Laboratory Animal Resource & Research Center > 1. Journal Articles
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