Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1994-9-20
pubmed:abstractText
The regulation of cytosolic Ca2+ concentration during excitation-contraction coupling is altered in the failing human heart. Previous studies have focused on disturbances in Ca2+ release and reuptake from the sarcoplasmic reticulum (SR), whereas functional studies of the cardiac Na(+)-Ca2+ exchanger, another important determinant of myocyte homeostasis, are lacking for the failing human heart. Using a cardiac Na(+)-Ca2+ exchanger cDNA recently cloned from a guinea pig cDNA library, we investigated the gene expression of the cardiac Na(+)-Ca2+ exchanger in relation to the SR Ca(2+)-ATPase. Expression of both genes was quantified in left ventricular myocardium from 24 failing human cardiac explants and 7 control heart samples in relation to beta-myosin heavy chain mRNA by slot blot analysis. Compared with patients with nonfailing hearts, patients with dilated cardiomyopathy (DCM, n = 13) showed a 55% increase in Na(+)-Ca2+ exchanger mRNA levels (P < .05 versus control value) and a 41% increase in patients with coronary artery disease (CAD, n = 11). In the same hearts, SR Ca(2+)-ATPase mRNA levels were decreased by 50% in DCM and by 45% in CAD (P < .05 for both versus control value). There was a positive correlation between Na(+)-Ca2+ exchanger and SR Ca(2+)-ATPase mRNA levels both in normal and failing human hearts, albeit with different slopes and intercepts of the regression line. The Na(+)-Ca2+ exchanger protein levels as assessed by Western blot analysis and normalized to beta-myosin heavy chain protein were increased in DCM and CAD (P < .05 and P < .01 versus control value, respectively), whereas SR Ca(2+)-ATPase protein levels were reduced (P < .05 for both groups versus control values). Thus, the Na(+)-Ca2+ exchanger gene expression is enhanced in failing human hearts and may, in part, compensate for the depressed SR function with regard to diastolic Ca2+ removal.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0009-7330
pubmed:author
pubmed:issnType
Print
pubmed:volume
75
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
443-53
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:8062418-Adult, pubmed-meshheading:8062418-Animals, pubmed-meshheading:8062418-Atrial Natriuretic Factor, pubmed-meshheading:8062418-Base Sequence, pubmed-meshheading:8062418-Blotting, Western, pubmed-meshheading:8062418-Calcium, pubmed-meshheading:8062418-Calcium-Transporting ATPases, pubmed-meshheading:8062418-Cardiomyopathy, Dilated, pubmed-meshheading:8062418-Carrier Proteins, pubmed-meshheading:8062418-Coronary Disease, pubmed-meshheading:8062418-Female, pubmed-meshheading:8062418-Gene Expression, pubmed-meshheading:8062418-Gene Library, pubmed-meshheading:8062418-Guinea Pigs, pubmed-meshheading:8062418-Humans, pubmed-meshheading:8062418-Male, pubmed-meshheading:8062418-Middle Aged, pubmed-meshheading:8062418-Molecular Sequence Data, pubmed-meshheading:8062418-Myocardium, pubmed-meshheading:8062418-Myosins, pubmed-meshheading:8062418-Oligodeoxyribonucleotides, pubmed-meshheading:8062418-RNA, Messenger, pubmed-meshheading:8062418-Rats, pubmed-meshheading:8062418-Reference Values, pubmed-meshheading:8062418-Restriction Mapping, pubmed-meshheading:8062418-Sarcoplasmic Reticulum, pubmed-meshheading:8062418-Sodium, pubmed-meshheading:8062418-Sodium-Calcium Exchanger
pubmed:year
1994
pubmed:articleTitle
Gene expression of the cardiac Na(+)-Ca2+ exchanger in end-stage human heart failure.
pubmed:affiliation
Arbeitsgruppe Molekulare Kardiologie, Universitat Freiburg, Germany.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't