Document Detail


Induced overexpression of Na(+)/Ca(2+) exchanger does not aggravate myocardial dysfunction induced by transverse aortic constriction.
MedLine Citation:
PMID:  23273595     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Alterations in expression and activity of cardiac Na(+)/Ca(2+) exchanger (NCX1) have been implicated in the pathogenesis of heart failure.
METHODS AND RESULTS: Using transgenic mice in which expression of rat NCX1 was induced at 5 weeks of age, we performed transverse aortic constriction (TAC) at 8 weeks and examined cardiac and myocyte function at 15-18 weeks after TAC (age 23-26 weeks). TAC induced left ventricular (LV) and myocyte hypertrophy and increased myocardial fibrosis in both wild-type (WT) and NCX1-overexpressed mice. NCX1 and phosphorylated ryanodine receptor expression was increased by TAC, whereas sarco(endo)plasmic reticulum Ca(2+)-ATPase levels were decreased by TAC. Action potential duration was prolonged by TAC, but to a greater extent in NCX1 myocytes. Na(+)/Ca(2+) exchange current was similar between WT-TAC and WT-sham myocytes, but was higher in NCX1-TAC myocytes. Both myocyte contraction and [Ca(2+)](i) transient amplitudes were reduced in WT-TAC myocytes, but restored to WT-sham levels in NCX1-TAC myocytes. Despite improvement in single myocyte contractility and Ca(2+) dynamics, induced NCX1 overexpression in TAC animals did not ameliorate LV hypertrophy, increase ejection fraction, or enhance inotropic (maximal first derivative of LV pressure rise, +dP/dt) responses to isoproterenol.
CONCLUSIONS: In pressure-overload hypertrophy, induced overexpression of NCX1 corrected myocyte contractile and [Ca(2+)](i) transient abnormalities but did not aggravate or improve myocardial dysfunction.
Authors:
Jufang Wang; Erhe Gao; Tung O Chan; Xue-Qian Zhang; Jianliang Song; Xiying Shang; Walter J Koch; Arthur M Feldman; Joseph Y Cheung
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cardiac failure     Volume:  19     ISSN:  1532-8414     ISO Abbreviation:  J. Card. Fail.     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2012-12-31     Completed Date:  2013-05-30     Revised Date:  2014-01-09    
Medline Journal Info:
Nlm Unique ID:  9442138     Medline TA:  J Card Fail     Country:  United States    
Other Details:
Languages:  eng     Pagination:  60-70     Citation Subset:  IM    
Copyright Information:
Copyright © 2013 Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Cells, Cultured
Constriction, Pathologic
Disease Models, Animal
Electrophysiology
Gene Expression Regulation
Heart Failure / genetics,  metabolism*,  pathology*
Immunoblotting
Male
Mice
Mice, Transgenic
Myocardial Contraction / physiology*
Myocytes, Cardiac / metabolism*
Patch-Clamp Techniques
Random Allocation
Rats
Reference Values
Sensitivity and Specificity
Sodium-Calcium Exchanger / genetics,  metabolism*
Grant Support
ID/Acronym/Agency:
P01 HL075443/HL/NHLBI NIH HHS; P01 HL091799/HL/NHLBI NIH HHS; P01-HL-75443/HL/NHLBI NIH HHS; P01-HL-91799/HL/NHLBI NIH HHS; P01-HL91799/HL/NHLBI NIH HHS; R01 HL056205/HL/NHLBI NIH HHS; R01 HL058672/HL/NHLBI NIH HHS; R01 HL074854/HL/NHLBI NIH HHS; R01 HL085503/HL/NHLBI NIH HHS; R01-HL56205/HL/NHLBI NIH HHS; R01-HL58672/HL/NHLBI NIH HHS; R01-HL61690/HL/NHLBI NIH HHS; R01-HL74854/HL/NHLBI NIH HHS; R01-HL85503/HL/NHLBI NIH HHS; R37 HL061690/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Sodium-Calcium Exchanger
Comments/Corrections

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