pubmed-article:17609291 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17609291 | lifeskim:mentions | umls-concept:C1416433 | lld:lifeskim |
pubmed-article:17609291 | lifeskim:mentions | umls-concept:C1266872 | lld:lifeskim |
pubmed-article:17609291 | lifeskim:mentions | umls-concept:C1171362 | lld:lifeskim |
pubmed-article:17609291 | lifeskim:mentions | umls-concept:C1564138 | lld:lifeskim |
pubmed-article:17609291 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
pubmed-article:17609291 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:17609291 | lifeskim:mentions | umls-concept:C1515670 | lld:lifeskim |
pubmed-article:17609291 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:17609291 | pubmed:dateCreated | 2007-8-31 | lld:pubmed |
pubmed-article:17609291 | pubmed:abstractText | Exposure of renal tubular epithelial cells (TEC) to IFN-gamma/TNF-alpha leads to Fas/FasL-mediated self-injury, which contributes to allograft rejection. Indoleamine 2,3-dioxygenase (IDO) converts tryptophan to N-formyl-kynurenine and contributes to immune privilege in tissues by increasing Fas-mediated T cell apoptosis. However, renal expression of IDO and its role in promoting Fas-mediated TEC death have not been examined. IDO expression was analyzed by RT-PCR and Western blot. Apoptosis was measured by fluorescence-activated cell sorting analysis and terminal deoxytransferase-mediated dUTP nick end labeling. We demonstrated that functional IDO is expressed in TEC and is increased by IFN-gamma/TNF-alpha exposure. Increased IDO activity promoted TEC apoptosis, whereas inhibition of IDO by its specific inhibitor 1-methyl-d-tryptophan attenuated IFN-gamma/TNF-alpha-mediated TEC apoptosis and augmented TEC survival. Transgenic expression of IDO resulted in increased TEC apoptosis in the absence of proinflammatory cytokine exposure, supporting a central role for IDO in TEC injury. Inhibition of IDO-mediated TEC death by a caspase-8-specific inhibitor (Z-IETD-FMK), as well as the absence of an IDO effect in Fas-deficient and FasL-deficient TEC, supports a Fas/FasL-dependent, caspase-8-mediated mechanism for IDO-enhanced TEC death. These data suggest that renal IDO expression may be deleterious during renal inflammation, because it enhances TEC self-injury through Fas/FasL interactions. Thus attenuation of IDO may represent a novel strategy to promote kidney function following ischemia and renal allograft rejection. | lld:pubmed |
pubmed-article:17609291 | pubmed:language | eng | lld:pubmed |
pubmed-article:17609291 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17609291 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:17609291 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17609291 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17609291 | pubmed:month | Sep | lld:pubmed |
pubmed-article:17609291 | pubmed:issn | 1931-857X | lld:pubmed |
pubmed-article:17609291 | pubmed:author | pubmed-author:DuCaiganC | lld:pubmed |
pubmed-article:17609291 | pubmed:author | pubmed-author:JevnikarAntho... | lld:pubmed |
pubmed-article:17609291 | pubmed:author | pubmed-author:DiaoHongH | lld:pubmed |
pubmed-article:17609291 | pubmed:author | pubmed-author:GuanQiunongQ | lld:pubmed |
pubmed-article:17609291 | pubmed:author | pubmed-author:MohibKanishka... | lld:pubmed |
pubmed-article:17609291 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17609291 | pubmed:volume | 293 | lld:pubmed |
pubmed-article:17609291 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17609291 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17609291 | pubmed:pagination | F801-12 | lld:pubmed |
pubmed-article:17609291 | pubmed:dateRevised | 2011-4-28 | lld:pubmed |
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pubmed-article:17609291 | pubmed:meshHeading | pubmed-meshheading:17609291... | lld:pubmed |
pubmed-article:17609291 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17609291 | pubmed:articleTitle | Proapoptotic activity of indoleamine 2,3-dioxygenase expressed in renal tubular epithelial cells. | lld:pubmed |
pubmed-article:17609291 | pubmed:affiliation | Department of Medicine and Microbiology, The University of Western Ontario, London, Ontario, Canada. | lld:pubmed |
pubmed-article:17609291 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17609291 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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