Key result
M-CK-deficient mouse hearts maintained significant Mi-CK flux during pacing, suggesting Mi-CK contributes more to total CK flux in wild-type hearts than the homodimeric M-CK isoform.
Mitochondrial creatine kinase contributes more significantly to total NMR-measured CK flux in wild-type hearts than the homodimeric M-CK isoform.
Mi-CK may predominate in cardiac CK flux; extends isoform energetics research in mice but leaves open human translation.
Hearts of wild-type and cytosolic muscle creatine kinase (M-CK)-knockout mice were perfused with Krebs-Henseleit buffer containing 10 mM glucose and 5 mM pyruvate and studied during pacing at 400 and 600 beats/min and during K+ arrest. Phosphocreatine (PCr) and ATP concentrations in M-CK-deficient hearts were not significantly different from those in wild-type hearts. With the use of 31P NMR saturation transfer, the flux mediated predominantly by mitochondrial creatine kinase (Mi-CK) was clearly detected in M-CK-deficient hearts. Mi-CK flux was 4.8 +/- 0.6 and 4.5 +/- 0.6 mM/s during pacing at 400 and 600 beats/min, respectively, and was 3. 5 +/- 0.4 mM/s during cardiac arrest. In control hearts total CK flux was 7.8 +/- 1.1 and 6.6 +/- 1.3 mM/s during pacing at 400 and 600 beats/min, respectively, and decreased to 3.8 +/- 0.5 mM/s during arrest. It is suggested that the relative contribution of Mi-CK to the total NMR-measured CK flux in the wild-type heart is higher than that of the homodimeric M-CK isoform (MM-CK).
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Dorsten et al. (1998) studied M-creatine kinase deficiency. M-CK knockout vs. Wild-type mice was evaluated on Creatine kinase flux. M-CK-deficient mouse hearts maintained significant Mi-CK flux during pacing, suggesting Mi-CK contributes more to total CK flux in wild-type hearts than the homodimeric M-CK isoform.
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