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dc.contributor.authorBisht, Kavita
dc.contributor.authorWegiel, Barbara
dc.contributor.authorTampe, Jens
dc.contributor.authorNeubauer, Oliver
dc.contributor.authorWagner, Karl-Heinz
dc.contributor.authorOtterbein, Leo E
dc.contributor.authorBulmer, Andrew C
dc.date.accessioned2017-12-19T01:00:51Z
dc.date.available2017-12-19T01:00:51Z
dc.date.issued2014
dc.date.modified2014-08-04T23:00:24Z
dc.identifier.issn0006-291X
dc.identifier.doi10.1016/j.bbrc.2014.04.150
dc.identifier.urihttp://hdl.handle.net/10072/61843
dc.description.abstractMacrophages play a crucial role in the maintenance and resolution of inflammation and express a number of pro- and anti-inflammatory molecules in response to stressors. Among them, the complement receptor 5a (C5aR) plays an integral role in the development of inflammatory disorders. Biliverdin and bilirubin, products of heme catabolism, exert anti-inflammatory effects and inhibit complement activation. Here, we define the effects of biliverdin on C5aR expression in macrophages and the roles of Akt and mammalian target of rapamycin (mTOR) in these responses. Biliverdin administration inhibited lipopolysaccharide (LPS)-induced C5aR expression (without altering basal expression), a effect partially blocked by rapamycin, an inhibitor of mTOR signaling. Biliverdin also reduced LPS-dependent expression of the pro-inflammatory cytokines TNF-a and IL-6. Collectively, these data indicate that biliverdin regulates LPS-mediated expression of C5aR via the mTOR pathway, revealing an additional mechanism underlying biliverdin's anti-inflammatory effects.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageEnglish
dc.language.isoeng
dc.publisherElsevier
dc.publisher.placeUnited States
dc.relation.ispartofstudentpublicationY
dc.relation.ispartofpagefrom94
dc.relation.ispartofpageto99
dc.relation.ispartofissue1
dc.relation.ispartofjournalBiochemical and Biophysical Research Communications
dc.relation.ispartofvolume449
dc.rights.retentionN
dc.subject.fieldofresearchBiological Sciences not elsewhere classified
dc.subject.fieldofresearchMedicinal and Biomolecular Chemistry
dc.subject.fieldofresearchBiochemistry and Cell Biology
dc.subject.fieldofresearchMedical Biochemistry and Metabolomics
dc.subject.fieldofresearchcode069999
dc.subject.fieldofresearchcode0304
dc.subject.fieldofresearchcode0601
dc.subject.fieldofresearchcode1101
dc.titleBiliverdin modulates the expression of C5aR in response to endotoxin in part via mTOR signaling
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.hasfulltextNo Full Text
gro.griffith.authorTampe, Jens
gro.griffith.authorBulmer, Andrew C.
gro.griffith.authorBisht, Kavita
gro.griffith.authorNeubauer, Oliver


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