Journal
EUROPEAN JOURNAL OF HEART FAILURE
Volume 12, Issue 12, Pages 1282-1289Publisher
WILEY
DOI: 10.1093/eurjhf/hfq174
Keywords
Heart failure; Energy metabolism; Adenylate kinase; Creatine kinase; Phosphotransfer
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Funding
- British Heart Foundation [RG/05/005]
- Wellcome Trust [075491/Z/04]
- MRC [G0600829] Funding Source: UKRI
- British Heart Foundation [RG/10/002/28187] Funding Source: researchfish
- Medical Research Council [G0600829] Funding Source: researchfish
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To measure the activity of the key phosphotransfer enzymes creatine kinase (CK), adenylate kinase (AK), and glycolytic enzymes in two common mouse models of chronic heart failure. C57BL/6 mice were subjected to transverse aortic constriction (TAC), myocardial infarction induced by coronary artery ligation (CAL), or sham operation. Activities of phosphotransfer enzymes CK, AK, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), 3-phosphoglycerate kinase (PGK), and pyruvate kinase were assessed spectrophotometrically. Mice were characterized by echocardiography or magnetic resonance imaging 5- to 8-week post-surgery and selected for the presence of congestive heart failure. All mice had severe left ventricular hypertrophy, impaired systolic function and pulmonary congestion compared with sham controls. A significant decrease in myocardial CK and maximal CK reaction velocity was observed in both experimental models of heart failure. However, the activity of AK and its isoforms remained unchanged, despite a reduction in its protein expression. In contrast, the activities of glycolytic phosphotransfer mediators GAPDH and PGK were 19 and 12% higher in TAC, and 31 and 23% higher in CAL models, respectively. Chronic heart failure in the mouse is characterized by impaired CK function, unaltered AK, and increased activity of glycolytic phosphotransfer enzymes. This pattern of altered phosphotransfer activity was observed independent of the heart failure aetiology.
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