Source:http://linkedlifedata.com/resource/pubmed/id/12490603
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2002-12-19
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| pubmed:abstractText |
Using Na+/Ca2+ exchanger (NCX1)-deficient mice, the pathophysiological role of Ca2+ overload via the reverse mode of NCX1 in ischemia/reperfusion-induced renal injury was investigated. Because NCX1(-/-) homozygous mice die of heart failure before birth, we used NCX1(+/-) heterozygous mice. NCX1 protein in the kidney of heterozygous mice decreased to about half of that of wild-type mice. Expression of NCX1 protein in the tubular epithelial cells and Ca2+ influx via NCX1 in renal tubules were markedly attenuated in the heterozygous mice. Ischemia/reperfusion-induced renal dysfunction in heterozygous mice was significantly attenuated compared with cases in wild-type mice. Histological renal damage such as tubular necrosis and proteinaceous casts in tubuli in heterozygous mice were much less than that in wild-type mice. Ca2+ deposition in necrotic tubular epithelium was observed more markedly in wild-type than in heterozygous mice. Increases in renal endothelin-1 content were greater in wild-type than in heterozygous mice, and this reflected the difference in immunohistochemical endothelin-1 localization in necrotic tubular epithelium. When the preischemic treatment with KB-R7943 was performed, the renal functional parameters of both NCX1(+/+) and NCX1(+/-) acute renal failure mice were improved to the same level. These findings strongly support the view that Ca2+ overload via the reverse mode of Na+/Ca2+ exchange, followed by renal endothelin-1 overproduction, plays an important role in the pathogenesis of ischemia/reperfusion-induced renal injury.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/2-(2-(4-(4-nitrobenzyloxy)phenyl)eth...,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Endothelin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Calcium Exchanger,
http://linkedlifedata.com/resource/pubmed/chemical/Thiourea,
http://linkedlifedata.com/resource/pubmed/chemical/sodium-calcium exchanger 1
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jan
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| pubmed:issn |
0022-3565
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| pubmed:author |
pubmed-author:IwamotoTakahiroT,
pubmed-author:KitaSatomiS,
pubmed-author:KomuroIsseiI,
pubmed-author:MatsumuraYasuoY,
pubmed-author:NishikawaMitsunoriM,
pubmed-author:OgataMasayaM,
pubmed-author:ShigekawaMunekazuM,
pubmed-author:TakaokaMasanoriM,
pubmed-author:TazawaNaokoN,
pubmed-author:WakimotoKojiK,
pubmed-author:YamashitaJunjiJ
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| pubmed:issnType |
Print
|
| pubmed:volume |
304
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
284-93
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:12490603-Animals,
pubmed-meshheading:12490603-Blood Urea Nitrogen,
pubmed-meshheading:12490603-Blotting, Western,
pubmed-meshheading:12490603-Calcium,
pubmed-meshheading:12490603-Cells, Cultured,
pubmed-meshheading:12490603-Endothelin-1,
pubmed-meshheading:12490603-Immunohistochemistry,
pubmed-meshheading:12490603-Kidney,
pubmed-meshheading:12490603-Kidney Diseases,
pubmed-meshheading:12490603-Kidney Function Tests,
pubmed-meshheading:12490603-Kidney Tubules, Distal,
pubmed-meshheading:12490603-Kidney Tubules, Proximal,
pubmed-meshheading:12490603-LLC-PK1 Cells,
pubmed-meshheading:12490603-Male,
pubmed-meshheading:12490603-Mice,
pubmed-meshheading:12490603-Mice, Knockout,
pubmed-meshheading:12490603-Reperfusion Injury,
pubmed-meshheading:12490603-Sodium-Calcium Exchanger,
pubmed-meshheading:12490603-Swine,
pubmed-meshheading:12490603-Thiourea,
pubmed-meshheading:12490603-Water-Electrolyte Balance
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| pubmed:year |
2003
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| pubmed:articleTitle |
Attenuation of ischemia/reperfusion-induced renal injury in mice deficient in Na+/Ca2+ exchanger.
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| pubmed:affiliation |
Department of Pharmacology, Osaka University of Pharmaceutical Sciences, Osaka, Japan.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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