| pubmed-article:19667249 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19667249 | lifeskim:mentions | umls-concept:C0022674 | lld:lifeskim |
| pubmed-article:19667249 | lifeskim:mentions | umls-concept:C0235989 | lld:lifeskim |
| pubmed-article:19667249 | lifeskim:mentions | umls-concept:C0023779 | lld:lifeskim |
| pubmed-article:19667249 | lifeskim:mentions | umls-concept:C0043316 | lld:lifeskim |
| pubmed-article:19667249 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:19667249 | lifeskim:mentions | umls-concept:C0220903 | lld:lifeskim |
| pubmed-article:19667249 | lifeskim:mentions | umls-concept:C0333668 | lld:lifeskim |
| pubmed-article:19667249 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:19667249 | pubmed:dateCreated | 2009-9-17 | lld:pubmed |
| pubmed-article:19667249 | pubmed:abstractText | Xanthine oxidoreductase (XOR) is an enzyme responsible for purine degradation, reactive oxygen species production, and adipogenesis. XOR gene-disrupted (XOR(-/-)) mice demonstrate renal failure and early death within several months. The aim of this study was to elucidate the mechanism of renal damage in XOR(-/-) mice and to determine the physiological role of XOR in the kidney. Histological analysis revealed that renal tubular damage in XOR(-/-) mice was accompanied by deposition of crystals and lipid-rich substances. Triglyceride content in renal homogenates was significantly increased in XOR(-/-) mice. The level of lipogenesis-related gene expression was comparable in XOR(+/+) and XOR(-/-) mice, whereas the expression of adipogenesis-related gene expression was significantly elevated in XOR(-/-) mice. Urinary excretions of xanthine and hypoxanthine were markedly elevated in XOR(-/-) mice. Immunohistochemical analysis, Western blotting, and real time RT-PCR revealed that various markers of fibrosis, inflammation, ischemia, and oxidative stress were increased in XOR(-/-) mice. Finally, we demonstrate that primary renal epithelial cells from XOR(-/-) mice are more readily transformed to myofibroblasts, which is a marker of increased epithelial mesenchymal transition. These results suggest that XOR gene disruption induced the depletion of uric acid and the accumulation of triglyceride-rich substances, xanthine, and hypoxanthine in the renal tubules. We believe that these changes contribute to a complex cellular milieu characterized by inflammation, tissue hypoxia, and reactive oxygen species production, ultimately resulting in renal failure through increased renal interstitial fibrosis. | lld:pubmed |
| pubmed-article:19667249 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19667249 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19667249 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19667249 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19667249 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19667249 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19667249 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19667249 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19667249 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19667249 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19667249 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19667249 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:19667249 | pubmed:issn | 1524-4563 | lld:pubmed |
| pubmed-article:19667249 | pubmed:author | pubmed-author:OhtsuboToshio... | lld:pubmed |
| pubmed-article:19667249 | pubmed:author | pubmed-author:FujiiKojiK | lld:pubmed |
| pubmed-article:19667249 | pubmed:author | pubmed-author:IidaMitsuoM | lld:pubmed |
| pubmed-article:19667249 | pubmed:author | pubmed-author:RoviraIlsa... | lld:pubmed |
| pubmed-article:19667249 | pubmed:author | pubmed-author:FinkelTorenT | lld:pubmed |
| pubmed-article:19667249 | pubmed:author | pubmed-author:MatsumuraKiyo... | lld:pubmed |
| pubmed-article:19667249 | pubmed:author | pubmed-author:TsuruyaKazuhi... | lld:pubmed |
| pubmed-article:19667249 | pubmed:author | pubmed-author:SakagamiKanae... | lld:pubmed |
| pubmed-article:19667249 | pubmed:author | pubmed-author:NoguchiHideko... | lld:pubmed |
| pubmed-article:19667249 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19667249 | pubmed:volume | 54 | lld:pubmed |
| pubmed-article:19667249 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19667249 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19667249 | pubmed:pagination | 868-76 | lld:pubmed |
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| pubmed-article:19667249 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19667249 | pubmed:articleTitle | Xanthine oxidoreductase depletion induces renal interstitial fibrosis through aberrant lipid and purine accumulation in renal tubules. | lld:pubmed |
| pubmed-article:19667249 | pubmed:affiliation | Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, Japan. tohtsubo@intmed2.med.kyushu-u.ac.jp | lld:pubmed |
| pubmed-article:19667249 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19667249 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:22436 | entrezgene:pubmed | pubmed-article:19667249 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:19667249 | lld:entrezgene |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:19667249 | lld:pubmed |
