Document Detail


Calcineurin-induced energy wasting in a transgenic mouse model of heart failure.
MedLine Citation:
PMID:  18192216     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Overexpression of calcineurin (CLN) in the mouse heart induces severe hypertrophy that progresses to heart failure, providing an opportunity to define the relationship between energetics and contractile performance in the severely failing mouse heart. Contractile performance was studied in isolated hearts at different pacing frequencies and during dobutamine challenge. Energetics were assessed by 31P-NMR spectroscopy as ATP and phosphocreatine concentrations ([ATP] and [PCr]) and free energy of ATP hydrolysis (|Delta G( approximately ATP)|). Mitochondrial and glycolytic enzyme activities, myocardial O2 consumption, and myocyte ultrastructure were determined. In transgenic (TG) hearts at all levels of work, indexes of systolic performance were reduced and [ATP] and capacity for ATP synthesis were lower than in non-TG hearts. This is the first report showing that myocardial [ATP] is lower in a TG mouse model of heart failure. [PCr] was also lower, despite an unexpected increase in the total creatine pool. Because Pi concentration remained low, despite lower [ATP] and [PCr], |Delta G( approximately ATP)| was normal; however, chemical energy did not translate to systolic performance. This was most apparent with beta-adrenergic stimulation of TG hearts, during which, for similar changes in |Delta G( approximately ATP)|, systolic pressure decreased, rather than increased. Structural abnormalities observed for sarcomeres and mitochondria likely contribute to decreased contractile performance. On the basis of the increases in enzyme activities of proteins important for ATP supply observed after treatment with the CLN inhibitor cyclosporin A, we also conclude that CLN directed inhibition of ATP-producing pathways in non-TG and TG hearts.
Authors:
Ilka Pinz; Sanford E Ostroy; Kirsten Hoyer; Hanna Osinska; Jeffrey Robbins; Jeffery D Molkentin; Joanne S Ingwall
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, N.I.H., Extramural     Date:  2008-01-11
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  294     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2008 Mar 
Date Detail:
Created Date:  2008-03-07     Completed Date:  2008-05-15     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1459-66     Citation Subset:  IM    
Affiliation:
NMR Laboratory for Physiological Chemistry, Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Diphosphate / metabolism
Adenosine Monophosphate / metabolism
Adenosine Triphosphate / metabolism
Animals
Calcineurin / pharmacology*
Creatine / metabolism
Energy Metabolism / drug effects*
Heart Failure / genetics,  metabolism*
Magnetic Resonance Spectroscopy
Mice
Mice, Transgenic
Microscopy, Electron
Myocytes, Cardiac / drug effects,  ultrastructure
Oxygen Consumption / drug effects
Phosphocreatine / metabolism
Grant Support
ID/Acronym/Agency:
HL-075619/HL/NHLBI NIH HHS; HL-52320/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
56-65-5/Adenosine Triphosphate; 57-00-1/Creatine; 58-64-0/Adenosine Diphosphate; 61-19-8/Adenosine Monophosphate; 67-07-2/Phosphocreatine; EC 3.1.3.16/Calcineurin

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


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