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dc.contributor.author Baek, K. ko
dc.contributor.author Park, H.-J. ko
dc.contributor.author Baek, J.-H. ko
dc.contributor.author Kim, Hyung Ryong ko
dc.date.available 2017-12-11T00:54:30Z -
dc.date.created 2017-12-07 -
dc.date.issued 2017-10 -
dc.identifier.citation International Journal of Molecular Sciences, v.18, no.10 -
dc.identifier.issn 1661-6596 -
dc.identifier.uri http://hdl.handle.net/20.500.11750/4750 -
dc.description.abstract Sympathetic nervous system stimulation-induced β-adrenergic signal transduction is known to induce bone loss and increase of osteoclast activity. Although isoproterenol, a nonspecific β-adrenergic receptor agonist, has been shown to increase receptor activator of NF-κB ligand (RANKL), the details of the regulatory mechanisms remain unclear. In the present study, we investigated the role of the nuclear factor of activated T-cells (NFAT) in isoproterenol-induced RANKL expression in C2C12 and in primary cultured mouse calvarial cells. Isoproterenol increased nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) and RANKL expressions at both mRNA and protein levels and increased NFAT reporter activity. NFATc1 knockdown blocked isoproterenolmediated RANKL expression. Isoproterenol also promoted cAMP response element-binding protein 1 (CREB1) and activating transcription factor 4 (ATF4) phosphorylation. Isoproterenolmediated transcriptional activation of NFAT was blocked by protein kinase A (PKA) inhibitor H89. Isoproterenol-induced CREB1, ATF4, NFATc1, and RANKL expressions were suppressed by H89. Mutations in cAMP response element-like or NFAT-binding element suppressed isoproterenolinduced RANKL promoter activity. Chromatin immunoprecipitation analysis demonstrated that isoproterenol increased NFAT-binding and ATF4-binding activities on the mouse RANKL promoter, but did not increase CREB1-binding activity. Association of NFATc1 and ATF4 was not observed in a co-immunoprecipitation study. ATF4 knockdown suppressed isoproterenol-induced NFAT binding to the RANKL promoter, whereas NFATc1 knockdown did not suppress isoproterenol-induced ATF4 binding to the RANKL promoter. ATF4 knockdown suppressed isoproterenol-induced expressions of NFATc1 and RANKL. These results suggest that isoproterenol increases RANKL expression in an ATF4/NFATc1-dependent manner. © 2017 by the author. Licensee MDPI, Basel, Switzerland. -
dc.language English -
dc.publisher Multidisciplinary Digital Publishing Institute (MDPI) -
dc.title Isoproterenol increases RANKL expression in a ATF4/NFATc1-dependent manner in mouse osteoblastic cells -
dc.type Article -
dc.identifier.doi 10.3390/ijms18102204 -
dc.identifier.wosid 000414671800186 -
dc.identifier.scopusid 2-s2.0-85032011668 -
dc.type.local Article(Overseas) -
dc.type.rims ART -
dc.description.journalClass 1 -
dc.contributor.nonIdAuthor Baek, K. -
dc.contributor.nonIdAuthor Park, H.-J. -
dc.contributor.nonIdAuthor Baek, J.-H. -
dc.identifier.citationVolume 18 -
dc.identifier.citationNumber 10 -
dc.identifier.citationTitle International Journal of Molecular Sciences -
dc.type.journalArticle Article -
dc.description.isOpenAccess Y -
dc.subject.keywordAuthor Activating transcription factor 4 (ATF4) -
dc.subject.keywordAuthor Isoproterenol -
dc.subject.keywordAuthor Nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) -
dc.subject.keywordAuthor RANKL transcription -
dc.subject.keywordAuthor β-adrenergic receptor -
dc.contributor.affiliatedAuthor Kim, Hyung Ryong -
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