Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:21436290rdf:typepubmed:Citationlld:pubmed
pubmed-article:21436290lifeskim:mentionsumls-concept:C0023516lld:lifeskim
pubmed-article:21436290lifeskim:mentionsumls-concept:C0022646lld:lifeskim
pubmed-article:21436290lifeskim:mentionsumls-concept:C0253023lld:lifeskim
pubmed-article:21436290lifeskim:mentionsumls-concept:C0035126lld:lifeskim
pubmed-article:21436290lifeskim:mentionsumls-concept:C0599946lld:lifeskim
pubmed-article:21436290lifeskim:mentionsumls-concept:C0332206lld:lifeskim
pubmed-article:21436290pubmed:issue4lld:pubmed
pubmed-article:21436290pubmed:dateCreated2011-4-1lld:pubmed
pubmed-article:21436290pubmed:abstractTextInflammation contributes to the pathogenesis of ischemic acute kidney injury (AKI), and T cells mediate the early phase of ischemia-reperfusion injury (IRI). The Fas/Fas ligand (FasL) pathway modulates the balance of T cell subsets in the peripheral circulation as well as multiple inflammatory responses, suggesting that FasL may mediate ischemic AKI. Here, we induced bilateral renal IRI in mice bearing a loss-of-function mutation of FasL (the gld mutation) and in wild-type mice. Compared with wild-type mice, serum creatinine was lower in gld mice (1.4 ± 0.9 mg/dl versus 2.6 ± 0.4) at 24 hours after IRI (P<0.05). In addition, gld mice had fewer TNF-?-producing T lymphocytes in the kidneys and renal lymph nodes. Furthermore, pharmacologic blockade of FasL protected the kidneys of wild-type mice from IRI. Analysis of bone marrow chimeric mice suggested that the pathogenic effect of FasL involves leukocytes; reconstitution of wild-type mice with gld splenocytes attenuated IRI. In contrast, reconstitution of gld mice with wild-type splenocytes enhanced IRI. These data demonstrate that FasL, particularly on leukocytes, mediates ischemic AKI.lld:pubmed
pubmed-article:21436290pubmed:languageenglld:pubmed
pubmed-article:21436290pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:21436290pubmed:citationSubsetIMlld:pubmed
pubmed-article:21436290pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:21436290pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:21436290pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:21436290pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:21436290pubmed:statusMEDLINElld:pubmed
pubmed-article:21436290pubmed:monthAprlld:pubmed
pubmed-article:21436290pubmed:issn1533-3450lld:pubmed
pubmed-article:21436290pubmed:authorpubmed-author:YagitaHideoHlld:pubmed
pubmed-article:21436290pubmed:authorpubmed-author:RabbHamidHlld:pubmed
pubmed-article:21436290pubmed:authorpubmed-author:RacusenLorrai...lld:pubmed
pubmed-article:21436290pubmed:authorpubmed-author:LiuManchangMlld:pubmed
pubmed-article:21436290pubmed:authorpubmed-author:HamadAbdel...lld:pubmed
pubmed-article:21436290pubmed:authorpubmed-author:WomerKarl LKLlld:pubmed
pubmed-article:21436290pubmed:authorpubmed-author:XiaoZuoxiangZlld:pubmed
pubmed-article:21436290pubmed:authorpubmed-author:HuangYanfeiYlld:pubmed
pubmed-article:21436290pubmed:authorpubmed-author:KoGang JeeGJlld:pubmed
pubmed-article:21436290pubmed:authorpubmed-author:JangHye...lld:pubmed
pubmed-article:21436290pubmed:authorpubmed-author:HigbeeElizabe...lld:pubmed
pubmed-article:21436290pubmed:copyrightInfoCopyright © 2011 by the American Society of Nephrologylld:pubmed
pubmed-article:21436290pubmed:issnTypeElectroniclld:pubmed
pubmed-article:21436290pubmed:volume22lld:pubmed
pubmed-article:21436290pubmed:ownerNLMlld:pubmed
pubmed-article:21436290pubmed:authorsCompleteYlld:pubmed
pubmed-article:21436290pubmed:pagination732-42lld:pubmed
pubmed-article:21436290pubmed:meshHeadingpubmed-meshheading:21436290...lld:pubmed
pubmed-article:21436290pubmed:meshHeadingpubmed-meshheading:21436290...lld:pubmed
pubmed-article:21436290pubmed:meshHeadingpubmed-meshheading:21436290...lld:pubmed
pubmed-article:21436290pubmed:meshHeadingpubmed-meshheading:21436290...lld:pubmed
pubmed-article:21436290pubmed:meshHeadingpubmed-meshheading:21436290...lld:pubmed
pubmed-article:21436290pubmed:meshHeadingpubmed-meshheading:21436290...lld:pubmed
pubmed-article:21436290pubmed:meshHeadingpubmed-meshheading:21436290...lld:pubmed
pubmed-article:21436290pubmed:meshHeadingpubmed-meshheading:21436290...lld:pubmed
pubmed-article:21436290pubmed:meshHeadingpubmed-meshheading:21436290...lld:pubmed
pubmed-article:21436290pubmed:meshHeadingpubmed-meshheading:21436290...lld:pubmed
pubmed-article:21436290pubmed:meshHeadingpubmed-meshheading:21436290...lld:pubmed
pubmed-article:21436290pubmed:meshHeadingpubmed-meshheading:21436290...lld:pubmed
pubmed-article:21436290pubmed:meshHeadingpubmed-meshheading:21436290...lld:pubmed
pubmed-article:21436290pubmed:meshHeadingpubmed-meshheading:21436290...lld:pubmed
pubmed-article:21436290pubmed:meshHeadingpubmed-meshheading:21436290...lld:pubmed
pubmed-article:21436290pubmed:meshHeadingpubmed-meshheading:21436290...lld:pubmed
pubmed-article:21436290pubmed:year2011lld:pubmed
pubmed-article:21436290pubmed:articleTitleBlocking Fas ligand on leukocytes attenuates kidney ischemia-reperfusion injury.lld:pubmed
pubmed-article:21436290pubmed:affiliationDivision of Nephrology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.lld:pubmed
pubmed-article:21436290pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:21436290pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
pubmed-article:21436290pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed
entrez-gene:14103entrezgene:pubmedpubmed-article:21436290lld:entrezgene
http://linkedlifedata.com/r...entrezgene:pubmedpubmed-article:21436290lld:entrezgene