| pubmed-article:20116427 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20116427 | lifeskim:mentions | umls-concept:C0175677 | lld:lifeskim |
| pubmed-article:20116427 | lifeskim:mentions | umls-concept:C1328818 | lld:lifeskim |
| pubmed-article:20116427 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
| pubmed-article:20116427 | lifeskim:mentions | umls-concept:C1545588 | lld:lifeskim |
| pubmed-article:20116427 | lifeskim:mentions | umls-concept:C1442161 | lld:lifeskim |
| pubmed-article:20116427 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:20116427 | pubmed:dateCreated | 2010-3-15 | lld:pubmed |
| pubmed-article:20116427 | pubmed:abstractText | In this study, mice lacking the gp91(phox) gene were used to address the role of NADPH oxidase in hyperhomocysteinemia-induced podocyte injury. It was found that a folate-free diet increased plasma homocysteine levels, but failed to increase O(2)(-) production in the glomeruli from gp91(phox) gene knockout (gp91(-/-)) mice, compared with wild-type (gp91(+/+)) mice. Proteinuria and glomerular damage index (GDI) were significantly lower, whereas the glomerular filtration rate (GFR) was higher in gp91(-/-) than in gp91(+/+) mice when they were on the folate-free diet (urine albumin excretion, 21.23+/-1.88 vs 32.86+/-4.03 microg/24 h; GDI, 1.17+/-0.18 vs 2.59+/-0.49; and GFR, 53.01+/-4.69 vs 40.98+/-1.44 microl/min). Hyperhomocysteinemia-induced decrease in nephrin expression and increase in desmin expression in gp91(+/+) mice were not observed in gp91(-/-) mice. Morphologically, foot process effacement and podocyte loss due to hyperhomocysteinemia were significantly attenuated in gp91(-/-) mice. In in vitro studies of podocytes, homocysteine was found to increase gp91(phox) expression and O2(*)(-) generation, which was substantially inhibited by gp91(phox) siRNA. Functionally, homocysteine-induced decrease in vascular endothelial growth factor-A production was abolished by gp91(phox) siRNA or diphenyleneiodonium, a NADPH oxidase inhibitor. These results suggest that the functional integrity of NADPH oxidase is essential for hyperhomocysteinemia-induced podocyte injury and glomerulosclerosis. | lld:pubmed |
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| pubmed-article:20116427 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20116427 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20116427 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20116427 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:20116427 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20116427 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:20116427 | pubmed:issn | 1873-4596 | lld:pubmed |
| pubmed-article:20116427 | pubmed:author | pubmed-author:ToyP LPL | lld:pubmed |
| pubmed-article:20116427 | pubmed:author | pubmed-author:ZhangChunC | lld:pubmed |
| pubmed-article:20116427 | pubmed:author | pubmed-author:LiPin-LanPL | lld:pubmed |
| pubmed-article:20116427 | pubmed:author | pubmed-author:BoiniKrishna... | lld:pubmed |
| pubmed-article:20116427 | pubmed:author | pubmed-author:HuJun-JunJJ | lld:pubmed |
| pubmed-article:20116427 | pubmed:author | pubmed-author:BrimsonChrist... | lld:pubmed |
| pubmed-article:20116427 | pubmed:author | pubmed-author:LaperleLaura... | lld:pubmed |
| pubmed-article:20116427 | pubmed:copyrightInfo | Copyright 2010 Elsevier Inc. All rights reserved. | lld:pubmed |
| pubmed-article:20116427 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20116427 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:20116427 | pubmed:volume | 48 | lld:pubmed |
| pubmed-article:20116427 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20116427 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20116427 | pubmed:pagination | 1109-17 | lld:pubmed |
| pubmed-article:20116427 | pubmed:dateRevised | 2011-7-28 | lld:pubmed |
| pubmed-article:20116427 | pubmed:meshHeading | pubmed-meshheading:20116427... | lld:pubmed |
| pubmed-article:20116427 | pubmed:meshHeading | pubmed-meshheading:20116427... | lld:pubmed |
| pubmed-article:20116427 | pubmed:meshHeading | pubmed-meshheading:20116427... | lld:pubmed |
| pubmed-article:20116427 | pubmed:meshHeading | pubmed-meshheading:20116427... | lld:pubmed |
| pubmed-article:20116427 | pubmed:meshHeading | pubmed-meshheading:20116427... | lld:pubmed |
| pubmed-article:20116427 | pubmed:meshHeading | pubmed-meshheading:20116427... | lld:pubmed |
| pubmed-article:20116427 | pubmed:meshHeading | pubmed-meshheading:20116427... | lld:pubmed |
| pubmed-article:20116427 | pubmed:meshHeading | pubmed-meshheading:20116427... | lld:pubmed |
| pubmed-article:20116427 | pubmed:meshHeading | pubmed-meshheading:20116427... | lld:pubmed |
| pubmed-article:20116427 | pubmed:meshHeading | pubmed-meshheading:20116427... | lld:pubmed |
| pubmed-article:20116427 | pubmed:meshHeading | pubmed-meshheading:20116427... | lld:pubmed |
| pubmed-article:20116427 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20116427 | pubmed:articleTitle | Protection of podocytes from hyperhomocysteinemia-induced injury by deletion of the gp91phox gene. | lld:pubmed |
