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Cited 14 time in webofscience Cited 16 time in scopus
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Novel involvement of miR-522-3p in high-mobility group box 1-induced prostaglandin reductase 1 expression and reduction of phagocytosis

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dc.contributor.authorKang, Gyeoung-Jin-
dc.contributor.authorLee, Hye-Ja-
dc.contributor.authorByun, Hyun Jung-
dc.contributor.authorKim, Eun Ji-
dc.contributor.authorKim, Hyun Ji-
dc.contributor.authorPark, Mi Kyung-
dc.contributor.authorLee, Chang-Hoon-
dc.date.accessioned2024-08-08T01:01:54Z-
dc.date.available2024-08-08T01:01:54Z-
dc.date.issued2017-04-
dc.identifier.issn0167-4889-
dc.identifier.issn1879-2596-
dc.identifier.urihttps://scholarworks.dongguk.edu/handle/sw.dongguk/14791-
dc.description.abstractResolution of inflammation is important for physiological homeostasis. Chronic inflammatory diseases may be caused by abnormal resolution of inflammation. However, what causes a failure of inflammatory resolution is unclear. Here we investigated the involvement of high mobility group box 1 (HMGB1) protein in the control of inflammatory resolution as an 'anti -resolution factor'. We first confirmed the increased expression of HMGB1 and prostaglandin reductase 1 (PTGR1) in inflammatory conditions and HMGB1-mediated regulation of the expression of PTGR1. The inhibition of phagocytosis by HMGB1 was abrogated by PTGR1 silencing. PTGR1 was a direct target of miR522-3p and its expression was regulated by miRNA-522-3p inhibitor or mimic. Finally, miR-522-3p had an important role in the regulation of PTGR1 expression by HMGB1. The data indicates that HMGB1-miR522-3p-PTGR1 axis may be involved in the abnormal resolution of inflammation and suggests that this mechanism might be a target for modulation of chronic inflammatory disorder. (C) 2017 Elsevier B.V. All rights reserved.-
dc.format.extent9-
dc.language영어-
dc.language.isoENG-
dc.publisherELSEVIER SCIENCE BV-
dc.titleNovel involvement of miR-522-3p in high-mobility group box 1-induced prostaglandin reductase 1 expression and reduction of phagocytosis-
dc.typeArticle-
dc.publisher.location네델란드-
dc.identifier.doi10.1016/j.bbamcr.2017.01.006-
dc.identifier.scopusid2-s2.0-85009724503-
dc.identifier.wosid000397362500002-
dc.identifier.bibliographicCitationBIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH, v.1864, no.4, pp 625 - 633-
dc.citation.titleBIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH-
dc.citation.volume1864-
dc.citation.number4-
dc.citation.startPage625-
dc.citation.endPage633-
dc.type.docTypeArticle-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClasssci-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaCell Biology-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryCell Biology-
dc.subject.keywordPlusBREAST-CANCER CELLS-
dc.subject.keywordPlusAPOPTOTIC NEUTROPHILS-
dc.subject.keywordPlusDOWN-REGULATION-
dc.subject.keywordPlusHMGB1-
dc.subject.keywordPlusRESOLUTION-
dc.subject.keywordPlusPROTEIN-
dc.subject.keywordPlusINFLAMMATION-
dc.subject.keywordPlusMICRORNA-
dc.subject.keywordPlusINACTIVATION-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordAuthorInflammation-
dc.subject.keywordAuthorHMGBI PTGR1-
dc.subject.keywordAuthormiR-522-3p-
dc.subject.keywordAuthorPhagocytosis-
dc.subject.keywordAuthorAntiresolution factor-
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