File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Altered sarcoplasmic reticulum Ca2+-ATPase gene expression in the human ventricle during end-stage heart failure

TitleAltered sarcoplasmic reticulum Ca2+-ATPase gene expression in the human ventricle during end-stage heart failure
Authors
Issue Date1990
Citation
Journal of Clinical Investigation, 1990, v. 85 n. 1, p. 305-309 How to Cite?
AbstractA decrease in the myocardial level of the mRNA encoding the Ca2+-ATPase of the sarcoplasmic reticulum (SR) has been recently reported during experimental cardiac hypertrophy and failure. To determine if such a deficit occurs in human end-stage heart failure, we compared the SR Ca2+-ATPase mRNA levels in left (LV) and right ventricular (RV) specimens from 13 patients undergoing cardiac transplantation (6 idiopathic dilated cardiomyopathies; 4 coronary artery diseases with myocardial infarctions; 3 diverse etiologies) with control heart samples using a rat cardiac SR Ca2+-ATPase cDNA probe. We observed a marked decrease in the mRNA for the Ca2+-ATP-ase relative to both the 18S ribosomal RNA and the myosin heavy chain mRNA in LV specimens of patients with heart failure compared to controls (-48%, P < 0.01 and -47%, P < 0.05, respectively). The LV ratio of Ca2+-ATPase mRNA to 18S RNA positively correlated with cardiac index (P < 0.02). The RV ratio correlated negatively with systolic, diastolic and mean pulmonary arterial pressures (P < 0.02, P < 0.02, and P < 0.01, respectively). We suggest that a decrease of the SR Ca2+-ATPase mRNA in the myocardium plays an important role in alterations of Ca2+ movements and myocardial relaxation reported during human end-stage heart failure.
Persistent Identifierhttp://hdl.handle.net/10722/195220
ISSN
2015 Impact Factor: 12.575
2015 SCImago Journal Rankings: 8.764
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMercadier, J-J-
dc.contributor.authorLompré, A-M-
dc.contributor.authorDuc, P-
dc.contributor.authorBoheler, KR-
dc.contributor.authorFraysse, J-B-
dc.contributor.authorWisnewsky, C-
dc.contributor.authorAllen, PD-
dc.contributor.authorKomajda, M-
dc.contributor.authorSchwartz, K-
dc.date.accessioned2014-02-25T01:40:19Z-
dc.date.available2014-02-25T01:40:19Z-
dc.date.issued1990-
dc.identifier.citationJournal of Clinical Investigation, 1990, v. 85 n. 1, p. 305-309-
dc.identifier.issn0021-9738-
dc.identifier.urihttp://hdl.handle.net/10722/195220-
dc.description.abstractA decrease in the myocardial level of the mRNA encoding the Ca2+-ATPase of the sarcoplasmic reticulum (SR) has been recently reported during experimental cardiac hypertrophy and failure. To determine if such a deficit occurs in human end-stage heart failure, we compared the SR Ca2+-ATPase mRNA levels in left (LV) and right ventricular (RV) specimens from 13 patients undergoing cardiac transplantation (6 idiopathic dilated cardiomyopathies; 4 coronary artery diseases with myocardial infarctions; 3 diverse etiologies) with control heart samples using a rat cardiac SR Ca2+-ATPase cDNA probe. We observed a marked decrease in the mRNA for the Ca2+-ATP-ase relative to both the 18S ribosomal RNA and the myosin heavy chain mRNA in LV specimens of patients with heart failure compared to controls (-48%, P < 0.01 and -47%, P < 0.05, respectively). The LV ratio of Ca2+-ATPase mRNA to 18S RNA positively correlated with cardiac index (P < 0.02). The RV ratio correlated negatively with systolic, diastolic and mean pulmonary arterial pressures (P < 0.02, P < 0.02, and P < 0.01, respectively). We suggest that a decrease of the SR Ca2+-ATPase mRNA in the myocardium plays an important role in alterations of Ca2+ movements and myocardial relaxation reported during human end-stage heart failure.-
dc.languageeng-
dc.relation.ispartofJournal of Clinical Investigation-
dc.titleAltered sarcoplasmic reticulum Ca2+-ATPase gene expression in the human ventricle during end-stage heart failure-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1172/JCI114429-
dc.identifier.pmid2136864-
dc.identifier.scopuseid_2-s2.0-0025169633-
dc.identifier.volume85-
dc.identifier.issue1-
dc.identifier.spage305-
dc.identifier.epage309-
dc.identifier.isiWOS:A1990CH52200043-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats