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Cited 26 time in webofscience Cited 29 time in scopus
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Atorvastatin and Simvastatin, but not Pravastatin, Up-regulate LPS-Induced MMP-9 Expression in Macrophages by Regulating Phosphorylation of ERK and CREB

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dc.contributor.authorLee, Dong Kun-
dc.contributor.authorPark, Eun Ju-
dc.contributor.authorKim, Eun Kyoung-
dc.contributor.authorJin, JunYup-
dc.contributor.authorKim, Jong Soo-
dc.contributor.authorShin, Ik Jae-
dc.contributor.authorKim, Bo-Yeon-
dc.contributor.authorLee, Hookeun-
dc.contributor.authorKim, Dong-Eog-
dc.date.available2020-02-29T09:47:21Z-
dc.date.created2020-02-05-
dc.date.issued2012-
dc.identifier.issn1015-8987-
dc.identifier.urihttps://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/17564-
dc.description.abstractStatins suppress expression of pro-inflammatory cytokines in endothelial cells, whereas they enhance it in immune cells. Pro-inflammatory cytokines and lipopolysaccharide (LPS) induce matrix metalloproteinase (MMP)-9 gene expression in macrophages, which has been linked to progress of various inflammatory diseases. The aim of this study was to identify effects of various statins on LPS-induced MMP-9 gene expression in macrophages and microglia. MMP-9 expression was analyzed by real-time PCR or zymography. Effect of statins on activation of signaling pathways was analyzed by time-dependent phosphorylation of signaling molecules. Atorvastatin and simvastatin, but not pravastatin, up-regulated LPS-induced MMP-9 expression in murine RAW 264.7 macrophages and BV2 microglia. The phosphorylation duration of extracellular signal regulated kinases was extended by simvastatin, but not by atorvastatin or pravastatin. The up-regulation of LPS-induced MMP-9 gene expression by the statins was dependent on extracellular calcium ions and mediated by enhancing phosphorylation of cAMP-responsive element binding protein. Geranylgeranyl pyrophosphate, a precursor for cholesterol synthesis, could suppress up-regulation of LPS-mediated MMP-9 gene expression by atorvastatin and simvastatin. Atorvastatin and simvastatin-mediated up-regulation of LPS-induced MMP-9 gene expression in macrophages and microglia in vitro raises an important concern about use of the widely-prescribed statins in certain inflammatory conditions that are mediated by LPS. Copyright (C) 2012 S. Karger AG, Basel-
dc.language영어-
dc.language.isoen-
dc.publisherKARGER-
dc.relation.isPartOfCELLULAR PHYSIOLOGY AND BIOCHEMISTRY-
dc.subjectFACTOR-KAPPA-B-
dc.subjectCOENZYME-A REDUCTASE-
dc.subjectMATRIX METALLOPROTEINASES-
dc.subjectENDOTHELIAL-CELLS-
dc.subjectALPHA PRODUCTION-
dc.subjectMATRIX-METALLOPROTEINASE-9-
dc.subjectINHIBITORS-
dc.subjectSTATINS-
dc.subjectGENE-
dc.subjectCHOLESTEROL-
dc.titleAtorvastatin and Simvastatin, but not Pravastatin, Up-regulate LPS-Induced MMP-9 Expression in Macrophages by Regulating Phosphorylation of ERK and CREB-
dc.typeArticle-
dc.type.rimsART-
dc.description.journalClass1-
dc.identifier.wosid000307533600001-
dc.identifier.doi10.1159/000341433-
dc.identifier.bibliographicCitationCELLULAR PHYSIOLOGY AND BIOCHEMISTRY, v.30, no.3, pp.499 - 511-
dc.identifier.scopusid2-s2.0-84863871129-
dc.citation.endPage511-
dc.citation.startPage499-
dc.citation.titleCELLULAR PHYSIOLOGY AND BIOCHEMISTRY-
dc.citation.volume30-
dc.citation.number3-
dc.contributor.affiliatedAuthorLee, Hookeun-
dc.type.docTypeArticle-
dc.subject.keywordAuthor&apos-
dc.subject.keywordAuthorCREB-
dc.subject.keywordAuthorERK-
dc.subject.keywordAuthorMacrophage-
dc.subject.keywordAuthorLPS-
dc.subject.keywordAuthorMMP-9-
dc.subject.keywordAuthorStatin-
dc.subject.keywordPlusFACTOR-KAPPA-B-
dc.subject.keywordPlusCOENZYME-A REDUCTASE-
dc.subject.keywordPlusMATRIX METALLOPROTEINASES-
dc.subject.keywordPlusENDOTHELIAL-CELLS-
dc.subject.keywordPlusALPHA PRODUCTION-
dc.subject.keywordPlusMATRIX-METALLOPROTEINASE-9-
dc.subject.keywordPlusINHIBITORS-
dc.subject.keywordPlusSTATINS-
dc.subject.keywordPlusGENE-
dc.subject.keywordPlusCHOLESTEROL-
dc.relation.journalResearchAreaCell Biology-
dc.relation.journalResearchAreaPhysiology-
dc.relation.journalWebOfScienceCategoryCell Biology-
dc.relation.journalWebOfScienceCategoryPhysiology-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
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