| pubmed-article:18495963 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18495963 | lifeskim:mentions | umls-concept:C0538674 | lld:lifeskim |
| pubmed-article:18495963 | lifeskim:mentions | umls-concept:C0151650 | lld:lifeskim |
| pubmed-article:18495963 | lifeskim:mentions | umls-concept:C0033414 | lld:lifeskim |
| pubmed-article:18495963 | lifeskim:mentions | umls-concept:C0011155 | lld:lifeskim |
| pubmed-article:18495963 | lifeskim:mentions | umls-concept:C1523298 | lld:lifeskim |
| pubmed-article:18495963 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:18495963 | pubmed:dateCreated | 2008-8-27 | lld:pubmed |
| pubmed-article:18495963 | pubmed:abstractText | Induction of heme oxygenase-1 (HO-1) is associated with potential antifibrogenic effects. The effects of HO-1 expression on epithelial-mesenchymal transition (EMT), which plays a critical role in the development of renal fibrosis, are unknown. In this study, HO-1(-/-) mice demonstrated significantly more fibrosis after 7 d of unilateral ureteral obstruction compared with wild-type mice, despite similar degrees of hydronephrosis. The obstructed kidneys of HO-1(-/-) mice also had greater macrophage infiltration and renal tubular TGF-beta1 expression than wild-type mice. In addition, the degree of EMT was more extensive in obstructed HO-1(-/-) kidneys, as assessed by alpha-smooth muscle actin and expression of S100A4 in proximal tubular epithelial cells. In vitro studies using proximal tubular cells isolated from HO-1(-/-) and wild-type kidneys confirmed these observations. In conclusion, HO-1 deficiency is associated with increased fibrosis, tubular TGF-beta1 expression, inflammation, and enhanced EMT in obstructive kidney disease. Modulation of the HO-1 pathway may provide a new therapeutic approach to progressive renal diseases. | lld:pubmed |
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| pubmed-article:18495963 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:18495963 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18495963 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18495963 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:18495963 | pubmed:issn | 1533-3450 | lld:pubmed |
| pubmed-article:18495963 | pubmed:author | pubmed-author:AgarwalAnupam... | lld:pubmed |
| pubmed-article:18495963 | pubmed:author | pubmed-author:KieJeong-HaeJ... | lld:pubmed |
| pubmed-article:18495963 | pubmed:author | pubmed-author:Hill-Kapturcz... | lld:pubmed |
| pubmed-article:18495963 | pubmed:author | pubmed-author:KapturczakMat... | lld:pubmed |
| pubmed-article:18495963 | pubmed:author | pubmed-author:TraylorAmieA | lld:pubmed |
| pubmed-article:18495963 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18495963 | pubmed:volume | 19 | lld:pubmed |
| pubmed-article:18495963 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18495963 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18495963 | pubmed:pagination | 1681-91 | lld:pubmed |
| pubmed-article:18495963 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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