pubmed-article:21436290 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:21436290 | lifeskim:mentions | umls-concept:C0023516 | lld:lifeskim |
pubmed-article:21436290 | lifeskim:mentions | umls-concept:C0022646 | lld:lifeskim |
pubmed-article:21436290 | lifeskim:mentions | umls-concept:C0253023 | lld:lifeskim |
pubmed-article:21436290 | lifeskim:mentions | umls-concept:C0035126 | lld:lifeskim |
pubmed-article:21436290 | lifeskim:mentions | umls-concept:C0599946 | lld:lifeskim |
pubmed-article:21436290 | lifeskim:mentions | umls-concept:C0332206 | lld:lifeskim |
pubmed-article:21436290 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:21436290 | pubmed:dateCreated | 2011-4-1 | lld:pubmed |
pubmed-article:21436290 | pubmed:abstractText | Inflammation 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:21436290 | pubmed:language | eng | lld:pubmed |
pubmed-article:21436290 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21436290 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:21436290 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21436290 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21436290 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21436290 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21436290 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:21436290 | pubmed:month | Apr | lld:pubmed |
pubmed-article:21436290 | pubmed:issn | 1533-3450 | lld:pubmed |
pubmed-article:21436290 | pubmed:author | pubmed-author:YagitaHideoH | lld:pubmed |
pubmed-article:21436290 | pubmed:author | pubmed-author:RabbHamidH | lld:pubmed |
pubmed-article:21436290 | pubmed:author | pubmed-author:RacusenLorrai... | lld:pubmed |
pubmed-article:21436290 | pubmed:author | pubmed-author:LiuManchangM | lld:pubmed |
pubmed-article:21436290 | pubmed:author | pubmed-author:HamadAbdel... | lld:pubmed |
pubmed-article:21436290 | pubmed:author | pubmed-author:WomerKarl LKL | lld:pubmed |
pubmed-article:21436290 | pubmed:author | pubmed-author:XiaoZuoxiangZ | lld:pubmed |
pubmed-article:21436290 | pubmed:author | pubmed-author:HuangYanfeiY | lld:pubmed |
pubmed-article:21436290 | pubmed:author | pubmed-author:KoGang JeeGJ | lld:pubmed |
pubmed-article:21436290 | pubmed:author | pubmed-author:JangHye... | lld:pubmed |
pubmed-article:21436290 | pubmed:author | pubmed-author:HigbeeElizabe... | lld:pubmed |
pubmed-article:21436290 | pubmed:copyrightInfo | Copyright © 2011 by the American Society of Nephrology | lld:pubmed |
pubmed-article:21436290 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:21436290 | pubmed:volume | 22 | lld:pubmed |
pubmed-article:21436290 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:21436290 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:21436290 | pubmed:pagination | 732-42 | lld:pubmed |
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pubmed-article:21436290 | pubmed:meshHeading | pubmed-meshheading:21436290... | lld:pubmed |
pubmed-article:21436290 | pubmed:year | 2011 | lld:pubmed |
pubmed-article:21436290 | pubmed:articleTitle | Blocking Fas ligand on leukocytes attenuates kidney ischemia-reperfusion injury. | lld:pubmed |
pubmed-article:21436290 | pubmed:affiliation | Division of Nephrology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. | lld:pubmed |
pubmed-article:21436290 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:21436290 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:21436290 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
entrez-gene:14103 | entrezgene:pubmed | pubmed-article:21436290 | lld:entrezgene |
http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:21436290 | lld:entrezgene |