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Am J Physiol Heart Circ Physiol 283: H680-H687, 2002. First published May 2, 2002; doi:10.1152/ajpheart.00800.2001
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Vol. 283, Issue 2, H680-H687, August 2002

Mitochondrial creatine kinase is critically necessary for normal myocardial high-energy phosphate metabolism

Matthias Spindler1, Reinhard Niebler1, Helga Remkes1, Michael Horn1, Titus Lanz2, and Stefan Neubauer1

1 Medizinische Universitätsklinik Würzburg, 97070 Würzburg; and 2 Physikalisches Institut der Universität Würzburg, 97080 Würzburg, Germany

The individual functional significance of the various creatine kinase (CK) isoenzymes for myocardial energy homeostasis is poorly understood. Whereas transgenic hearts lacking the M subunit of CK (M-CK) show unaltered cardiac energetics and left ventricular (LV) performance, deletion of M-CK in combination with loss of sarcomeric mitochondrial CK (ScCKmit) leads to significant alterations in myocardial high-energy phosphate metabolites. To address the question as to whether this alteration is due to a decrease in total CK activity below a critical threshold or due to the specific loss of ScCKmit, we studied isolated perfused hearts with selective loss of ScCKmit (ScCKmit-/-, remaining total CK activity ~70%) using 31P NMR spectroscopy at two different workloads. LV performance in ScCKmit-/- hearts (n = 11) was similar compared with wild-type hearts (n = 9). Phosphocreatine/ATP, however, was significantly reduced in ScCKmit-/- compared with wild-type hearts (1.02 ± 0.05 vs. 1.54 ± 0.07, P < 0.05). In parallel, free [ADP] was higher (144 ± 11 vs. 67 ± 7 µM, P < 0.01) and free energy release for ATP hydrolysis (Delta GATP) was lower (-55.8 ± 0.5 vs. -58.5 ± 0.5 kJ/mol, P < 0.01) in ScCKmit-/- compared with wild-type hearts. These results demonstrate that M- and B-CK containing isoenzymes are unable to fully substitute for the loss of ScCKmit. We conclude that ScCKmit, in contrast to M-CK, is critically necessary to maintain normal high-energy phosphate metabolite levels in the heart.

creatine kinase; energy metabolism; nuclear magnetic resonance spectroscopy; transgenic mouse


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