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Interleukin-13 enhances cyclooxygenase-2 expression in activated rat brain microglia: implications for death of activated microglia.

DC Field Value Language
dc.contributor.authorYang, MS-
dc.contributor.authorJi, KA-
dc.contributor.authorJeon, SB-
dc.contributor.authorJin, BK-
dc.contributor.authorKim, SU-
dc.contributor.authorJou, I-
dc.contributor.authorJoe, E-
dc.date.accessioned2011-03-24T01:27:12Z-
dc.date.available2011-03-24T01:27:12Z-
dc.date.issued2006-
dc.identifier.issn0022-1767-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/1910-
dc.description.abstractBrain inflammation has recently attracted widespread interest because it is a risk factor for the onset and progression of brain diseases. In this study, we report that cyclooxygenase-2 (COX-2) plays a key role in the resolution of brain inflammation by inducing the death of microglia. We previously reported that IL-13, an anti-inflammatory cytokine, induced the death of activated microglia. These results revealed that IL-13 significantly enhanced COX-2 expression and production of PGE(2) and 15-deoxy-Delta(12,14)-PGJ(2) (15d-PGJ(2)) in LPS-treated microglia. Two other anti-inflammatory cytokines, IL-10 and TGF-beta, neither induced microglial death nor enhanced COX-2 expression or PGE(2) or 15d-PGJ(2) production. Therefore, we hypothesized that the effect of IL-13 on COX-2 expression may be linked to death of activated microglia. We found that COX-2 inhibitors (celecoxib and NS398) suppressed the death of microglia induced by a combination of LPS and IL-13 and that exogenous addition of PGE(2) and 15d-PGJ(2) induced microglial death. Agonists of EP2 (butaprost) and peroxisome proliferator-activated receptor gamma (ciglitazone) mimicked the effect of PGE(2) and 15d-PGJ(2), and an EP2 antagonist (AH6809) and a peroxisome proliferator-activated receptor gamma antagonist (GW9662) suppressed microglial death induced by LPS in combination with IL-13. In addition, IL-13 potentiated LPS-induced activation of JNK, and the JNK inhibitor SP600125 suppressed the enhancement of COX-2 expression and attenuated microglial death. Taken together, these results suggest that IL-13 enhanced COX-2 expression in LPS-treated microglia through the enhancement of JNK activation. Furthermore, COX-2 products, PGE(2) and 15d-PGJ(2), caused microglial death, which terminates brain inflammation.-
dc.language.isoen-
dc.subject.MESHAnimals-
dc.subject.MESHBrain-
dc.subject.MESHCell Death-
dc.subject.MESHCells, Cultured-
dc.subject.MESHCyclooxygenase 2-
dc.subject.MESHInterleukin-10-
dc.subject.MESHInterleukin-13-
dc.subject.MESHInterleukin-4-
dc.subject.MESHJNK Mitogen-Activated Protein Kinases-
dc.subject.MESHLipopolysaccharides-
dc.subject.MESHMicroglia-
dc.subject.MESHPPAR gamma-
dc.subject.MESHRats-
dc.subject.MESHRats, Sprague-Dawley-
dc.subject.MESHReceptors, Prostaglandin E-
dc.subject.MESHReceptors, Prostaglandin E, EP2 Subtype-
dc.subject.MESHTransforming Growth Factor beta-
dc.subject.MESHUp-Regulation-
dc.titleInterleukin-13 enhances cyclooxygenase-2 expression in activated rat brain microglia: implications for death of activated microglia.-
dc.typeArticle-
dc.identifier.pmid16818793-
dc.identifier.urlhttp://www.jimmunol.org/cgi/pmidlookup?view=long&pmid=16818793-
dc.contributor.affiliatedAuthor양, 명순-
dc.contributor.affiliatedAuthor진, 병관-
dc.contributor.affiliatedAuthor김, 승업-
dc.contributor.affiliatedAuthor주, 일로-
dc.contributor.affiliatedAuthor조, 은혜-
dc.type.localJournal Papers-
dc.citation.titleJournal of immunology (Baltimore, Md. : 1950)-
dc.citation.volume177-
dc.citation.number2-
dc.citation.date2006-
dc.citation.startPage1323-
dc.citation.endPage1329-
dc.identifier.bibliographicCitationJournal of immunology (Baltimore, Md. : 1950), 177(2). : 1323-1329, 2006-
dc.identifier.eissn1550-6606-
dc.relation.journalidJ000221767-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
Journal Papers > Research Organization > Institute for Medical Sciences
Journal Papers > School of Medicine / Graduate School of Medicine > Neurology
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