Please use this identifier to cite or link to this item: https://scholarhub.balamand.edu.lb/handle/uob/2695
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dc.contributor.authorTakahasi, Yujien_US
dc.contributor.authorIsuzugawa, Kazutoen_US
dc.contributor.authorMurase, Yasunorien_US
dc.contributor.authorImai, Misaen_US
dc.contributor.authorYamamoto, Shinyaen_US
dc.contributor.authorIizuka, Masateruen_US
dc.contributor.authorAkira, Shizuoen_US
dc.contributor.authorBahr, George M.en_US
dc.contributor.authorMomotani, Ei-ichien_US
dc.contributor.authorHori, Masatoshien_US
dc.contributor.authorOzaki, Hiroshien_US
dc.contributor.authorImakawa, Kazuhikoen_US
dc.date.accessioned2020-12-23T09:18:34Z-
dc.date.available2020-12-23T09:18:34Z-
dc.date.issued2006-
dc.identifier.urihttps://scholarhub.balamand.edu.lb/handle/uob/2695-
dc.description.abstractNOD1 (Card4) and NOD2 (Card15) are thought to be responsible for cytoplasmic defense against bacterial entry. To gain further knowledge about how their expressions are regulated in murine macrophages, we investigated the expression of NOD1 and NOD2 mRNAs after stimulation with various endotoxins, lipopolysaccharide, lipoteichoic acid and peptidoglycan. In macrophage RAW264.7 cells, the first and second rises in NOD1 and NOD2 mRNAs were observed at 2 hr and at 8-12 hr after endotoxin treatment. Increases in NOD1 and NOD2 mRNAs at 2 hr in lipopolysaccharide-treated RAW264.7 cells were reduced with the use of NF-κB inhibitor, caffeic acid phenetyl ester. In RAW264.7 cells, lipopolysaccharide-induced increases in NOD1 and NOD2 mRNAs were inhibited with anti-TLR4 antibody, and partially reduced in peritoneal macrophages obtained from TLR4-deficient mice. Furthermore, NOD1 and NOD2 mRNA expressions in RAW264.7 cells were increased by the treatment with proinflammatory cytokines, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), or IL-6. In TNF-α deficient macrophages, the expression of NOD molecules was minimal at 12 hr, and the second rise in NOD mRNA seen in lipopolysaccharide-treated RAW264.7 cells was inhibited with anti-TNF-α, but not with anti-IL-1β or anti-IL-6 antibody. These observations suggest that immediate response of NODs to endotoxins could result from NF-κB activation via TLR signaling, whereas the second rise in NOD mRNAs might have resulted from TNF-α production possibly through NF-κB, TLR, and/or NOD signalings.en_US
dc.format.extent7 p.en_US
dc.language.isoengen_US
dc.subjectMurineen_US
dc.subjectNOD1en_US
dc.subjectNOD2en_US
dc.subjectTNF-αen_US
dc.subject.lcshMacrophagesen_US
dc.titleUp-Regulation of NOD1 and NOD2 through TLR4 and TNF- alpha in LPS-treated Murine Macrophagesen_US
dc.typeJournal Articleen_US
dc.contributor.affiliationFaculty of Medicineen_US
dc.description.volume68en_US
dc.description.issue5en_US
dc.description.startpage471en_US
dc.description.endpage478en_US
dc.date.catalogued2017-11-14-
dc.description.statusPublisheden_US
dc.identifier.OlibID174970-
dc.identifier.openURLhttps://www.jstage.jst.go.jp/article/jvms/68/5/68_5_471/_pdfen_US
dc.relation.ispartoftextJournal of veterinary medical scienceen_US
dc.provenance.recordsourceOliben_US
Appears in Collections:Faculty of Medicine
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