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Titolo:
Downregulation of the Na+-creatine cotransporter in failing human myocardium and in experimental heart failure
Autore:
Neubauer, S; Remkes, H; Spindler, M; Horn, M; Wiesmann, F; Prestle, J; Walzel, B; Ertl, G; Hasenfuss, G; Wallimann, T;
Indirizzi:
Univ Wurzburg, Med Klin, D-97080 Wurzburg, Germany Univ Wurzburg Wurzburg Germany D-97080 d Klin, D-97080 Wurzburg, Germany Univ Gottingen, Abt Mol Kardiol, D-3400 Gottingen, Germany Univ GottingenGottingen Germany D-3400 rdiol, D-3400 Gottingen, Germany ETH Honggerberg, Inst Cell Biol, CH-8093 Zurich, Switzerland ETH Honggerberg Zurich Switzerland CH-8093 , CH-8093 Zurich, Switzerland
Titolo Testata:
CIRCULATION
fascicolo: 18, volume: 100, anno: 1999,
pagine: 1847 - 1850
SICI:
0009-7322(19991102)100:18<1847:DOTNCI>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENERGY-METABOLISM; SKELETAL-MUSCLE; KINASE SYSTEM; TRANSPORTER; INFARCTION; RAT; EXPRESSION; TISSUES; KIDNEY; BRAIN;
Keywords:
sodium; creatine; myocardium; heart failure;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
18
Recensione:
Indirizzi per estratti:
Indirizzo: Neubauer, S Univ Wurzburg, Med Klin, Josef Schneider Str 2, D-97080 Wurzburg, Germany Univ Wurzburg Josef Schneider Str 2 Wurzburg Germany D-97080
Citazione:
S. Neubauer et al., "Downregulation of the Na+-creatine cotransporter in failing human myocardium and in experimental heart failure", CIRCULATION, 100(18), 1999, pp. 1847-1850

Abstract

Background-The failing myocardium is characterized by depletion of phosphocreatine and of total creatine content. We hypothesized that this is due toloss of creatine transporter:protein. Methods and Results-Creatine transporter protein was quantified in nonfailing and failing human myocardium (explanted hearts with dilated cardiomyopathy [DCM; n = 8] and healthy donor,hearts [n = 8]) as well as in experimental heart failure (residual intact left ventricular tissue, rats 2 months after left anterior descending coronary artery ligation [MI; n = 8] of sham operation [sham; n = 6]) by Western blotting. Total creatine content was determined by high-performance liquid chromatography. Donor and DCM hearts hadtotal creatine contents of 136.4 +/- 6.1 and 68.7 +/- 4.6 nmol/mg protein,respectively (*P < 0.05); creatine transporter protein was 25.4 +/- 2.2 optical density units in donor and 17.7 +/- 2.5 in DCM (*P < 0.05). Total creatine was 87.5 +/- 4.2 nmol/mg protein in sham and 65.7 +/- 4.2 in MI rats (*P < 0.05); creatine transporter protein was 139.0 +/- 8.7 optical densityunits in sham and 821 +/- 4.0 in MI (*P < 0.05). Conclusions-Both in human and in experimental heart failure, creatine transporter protein content is reduced. This mechanism may contribute to the depletion of creatine compounds and thus to the reduced energy reserve in failing myocardium. This finding may have therapeutic implications, suggestinga search for treatment strategies targeted toward creatine transport.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/09/20 alle ore 23:10:53