Source:http://linkedlifedata.com/resource/pubmed/id/16309585
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2005-11-28
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pubmed:abstractText |
Transforming growth factor-beta (TGF-beta) is implicated in a variety of kidney diseases where it promotes extracellular matrix (ECM) deposition and pro-inflammatory events, but it also stabilizes and attenuates tissue injury through the activation of cytoprotective proteins, including heme oxygenase-1 (HO-1). HO-1 catalyzes the conversion of heme into carbon monoxide (CO), iron, and biliverdin, which is subsequently converted to bilirubin. The beneficial effects of HO-1 induction include decreasing pro-oxidants (heme), increasing anti-oxidants (biliverdin and bilirubin), and producing a vasodilator with anti-apoptotic and anti-inflammatory properties (CO). The reaction products of HO-1 may also have antifibrogenic properties. The purpose of this study is to explore the effects of HO-1 expression and its reaction products on fibronectin, an ECM protein, in the kidney. The results demonstrate that kidneys of HO-1 knockout mice express significantly more fibronectin protein as compared to heterozygote mice. A potent inducer of HO-1, hemin, significantly decreases fibronectin protein with a concomitant increase in HO-1 protein. Cells expressing HO-1, via TGF-beta1 induction, have reduced fibronectin expression. Bilirubin, a product of the heme oxygenase reaction, attenuates TGF-beta1-mediated increases in fibronectin expression. These results indicate that HO-1 induction and activity may modulate the production of ECM components and suggest a potential role for TGF-beta-mediated HO-1 induction in attenuating renal fibrosis.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1165-158X
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
30
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pubmed:volume |
51
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
357-62
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pubmed:dateRevised |
2007-12-3
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pubmed:meshHeading |
pubmed-meshheading:16309585-Animals,
pubmed-meshheading:16309585-Bilirubin,
pubmed-meshheading:16309585-Cell Line,
pubmed-meshheading:16309585-Enzyme Induction,
pubmed-meshheading:16309585-Epithelial Cells,
pubmed-meshheading:16309585-Fibronectins,
pubmed-meshheading:16309585-Fibrosis,
pubmed-meshheading:16309585-Heme Oxygenase-1,
pubmed-meshheading:16309585-Kidney Tubules,
pubmed-meshheading:16309585-Male,
pubmed-meshheading:16309585-Mice,
pubmed-meshheading:16309585-Mice, Knockout,
pubmed-meshheading:16309585-Transforming Growth Factor beta
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pubmed:year |
2005
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pubmed:articleTitle |
Induction of heme oxygenase-1 modulates the profibrotic effects of transforming growth factor-beta in human renal tubular epithelial cells.
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pubmed:affiliation |
Department of Medicine, Nephrology Research and Training Center, University of Alabama, Birmingham, AL 35294-0001, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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