Document Detail


Exercise training improves cardiac function and attenuates arrhythmia in CPVT mice.
MedLine Citation:
PMID:  23042908     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a lethal ventricular arrhythmia evoked by physical or emotional stress. Recessively inherited CPVT is caused by either missense or null-allele mutations in the cardiac calsequestrin (CASQ2) gene. It was suggested that defects in CASQ2 cause protein deficiency and impair Ca(2+) uptake to the sarcoplasmic reticulum and Ca(2+)-dependent inhibition of ryanodine channels, leading to diastolic Ca(2+) leak, after-depolarizations, and arrhythmia. To examine the effect of exercise training on left ventricular remodeling and arrhythmia, CASQ2 knockout (KO) mice and wild-type controls underwent echocardiography and heart rhythm telemetry before and after 6 wk of training by treadmill exercise. qRT-PCR and Western blotting were used to measure gene and protein expression. Left ventricular fractional shortening was impaired in KO (33 ± 5 vs. 51 ± 7% in controls, P < 0.05) and improved after training (43 ± 12 and 51 ± 9% in KO and control mice, respectively, P = nonsignificant). The exercise tolerance was low in KO mice (16 ± 1 vs. 29 ± 2 min in controls, P < 0.01), but improved in trained animals (26 ± 2 vs. 30 ± 3 min, P = nonsignificant). The hearts of KO mice had a higher basal expression of the brain natriuretic peptide gene. After training, the expression of natriuretic peptide genes markedly decreased, with no difference between KO and controls. Exercise training was not associated with a change in ventricular tachycardia prevalence, but appeared to reduce arrhythmia load, as manifested by a decrease in ventricular beats during stress. We conclude that, in KO mice, which recapitulate the phenotype of human CPVT2, exercise training is well tolerated and could offer a strategy for heart conditioning against stress-induced arrhythmia.
Authors:
Efrat Kurtzwald-Josefson; Edith Hochhauser; Guy Katz; Eyal Porat; Jonathan G Seidman; Christine E Seidman; Yelena Chepurko; Asher Shainberg; Michael Eldar; Michael Arad
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-10-04
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  113     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-12-03     Completed Date:  2013-05-29     Revised Date:  2013-12-04    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1677-83     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Atrial Natriuretic Factor / genetics,  metabolism
Blotting, Western
Calsequestrin / deficiency,  genetics
Disease Models, Animal
Exercise Therapy*
Exercise Tolerance
Gene Expression Regulation
Genetic Predisposition to Disease
Male
Mice
Mice, Knockout
Myocardial Contraction
Myocardium / metabolism
Natriuretic Peptide, Brain / genetics,  metabolism
Phenotype
RNA, Messenger / metabolism
Real-Time Polymerase Chain Reaction
Recovery of Function
Reverse Transcriptase Polymerase Chain Reaction
Tachycardia, Ventricular / genetics,  metabolism,  physiopathology,  therapy*
Time Factors
Ventricular Function, Left*
Ventricular Remodeling
Grant Support
ID/Acronym/Agency:
R01 HL080494/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Calsequestrin; 0/RNA, Messenger; 0/casq2 protein, mouse; 114471-18-0/Natriuretic Peptide, Brain; 85637-73-6/Atrial Natriuretic Factor
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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