Signaling and expression for mitochondrial membrane proteins during left ventricular remodeling and contractile failure after myocardial infarction

Xue Han Ning, Jianyi J Zhang, Jingbo Liu, Yun Ye, Shi Han Chen, Arthur H From, Robert J Bache, Michael A. Portman

Research output: Contribution to journalArticlepeer-review

49 Scopus citations


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 to normal (n = 8) occur in CHF, p < 0.01, but not in LVR. Relative expression for both proteins coordinated with their respective steady-state mRNA levels; CHF at 40% normal, p < 0.05 for ANT and 70% normal for betaF1, p < 0.05. Conclusions. Maintained signaling for major mitochondrial membrane proteins occurs in association with successful remodeling and adaptation after infarction. Reduced expression of these proteins relates to limited ATP synthesis capacity and high energy phosphate kinetic abnormalities previously demonstrated in CHF. These findings imply that mitochondrial processes participate in myocardial remodeling after infarction. (C) 2000 by the American College of Cardiology.

Original languageEnglish (US)
Pages (from-to)282-287
Number of pages6
JournalJournal of the American College of Cardiology
Issue number1
StatePublished - Jul 2000

Bibliographical note

Funding Information:
This work was supported by U.S. Public Health Service Grants HL 60666, HL21872, HL33600 and HL50470.


Dive into the research topics of 'Signaling and expression for mitochondrial membrane proteins during left ventricular remodeling and contractile failure after myocardial infarction'. Together they form a unique fingerprint.

Cite this