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Am J Physiol Heart Circ Physiol (May 2, 2002). doi:10.1152/ajpheart.00800.2001
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Articles in PresS, published online ahead of print May 2, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00800.2001
Submitted on September 12, 2001
Accepted on April 19, 2002

Mitochondrial Creatine Kinase is Critically Necessary to Maintain a Normal Profile of Myocardial High Energy Phosphate Metabolites

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

1 Medicine, Wuerzburg University, Wuerzburg, Germany
2 Physics, Wuerzburg University, Wuerzburg, Germany

* To whom correspondence should be addressed. E-mail: spindler{at}mail.uni-wuerzburg.de.

The individual functional significance of the various creatine kinase (CK) isoenzymes for myocardial energy homeostasis is poorly understood. Whereas transgenic hearts lacking M-CK show unaltered cardiac energetics and left ventricular (LV) performance, deletion of M-CK in combination with loss of 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 31PNMR spectroscopy at two different workloads. LV performance in ScCKmit-/- (n=11) was similar compared to wildtype hearts (n=9). PCr/ATP, however, was significantly reduced in ScCKmit-/- compared to wildtype (1.02±0.05 vs 1.54±0.07, p<0.05). In parallel, free ADP concentration 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 to wildtype 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 heart.




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