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Signaling and Expression for Mitochondrial Membrane Proteins During Left Ventricular Remodeling and

By Contractile Failure, After Myocardial Infarction and Michael A. Portman


OBJECTIVES This study was conducted to test hypotheses stating that: 1) altered signaling for mitochondrial membrane proteins occurs during postinfarction remodeling, and 2) successful myocardial adaptation relates to promotion of specific mitochondrial membrane components. BACKGROUND Abnormalities in high-energy phosphate content and limitations in adenosine 5�triphosphate (ATP) synthesis rate occur during the transition to contractile failure from compensatory remodeling after left ventricular infarction. The adenine nucleotide translocator (ANT) and F1-ATPase respectively regulate mitochondrial adenosine 5�-diphosphate (ADP)/ATP exchange and ADP-phosphorylation, which are key components of high-energy phosphate metabolism. METHODS Steady-state mRNA and protein expression for ANT isoform1 and the beta subunit of the F1-ATPase (betaF1) were analyzed in myocardium remote from the infarction zone eight weeks after left circumflex coronary artery ligation in pigs, demonstrating either successful left ventricular remodeling (LVR, n � 8) or congestive heart failure (CHF, n � 4) as determined by clinical and contractile performance parameters. RESULTS Substantial reductions in steady-state mRNA expression for ANT1 and betaF1 relative t

Year: 2013
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