TY - JOUR
T1 - Muscle creatine kinase-deficient mice
T2 - II. Cardiac and skeletal muscles exhibit tissue-specific adaptation of the mitochondrial function
AU - Veksler, Vladimir I.
AU - Kuznetsov, Andrey V.
AU - Anflous, Keltoum
AU - Mateo, Philippe
AU - Van Deursen, Jan
AU - Wieringa, Bé
AU - Ventura-Clapier, Renée
PY - 1995/8/25
Y1 - 1995/8/25
N2 - Functional properties of in situ mitochondria and of mitochondrial creatine kinase were studied in saponin-skinned fibers taken from normal and M-creatine kinase-deficient mice. In control animals, apparent Km values of mitochondrial respiration for ADP in cardiac (ventricular) and slow-twitch (soleus) muscles (137 ± 16 μM and 209 ± 10 μM, respectively) were manyfold higher than that in fast-twitch (gastrocnemius) muscle (7.5 ± 0.5 μM). Creatine substantially decreased the Km values only in cardiac and slow-twitch muscles (73 ± 11 μM and 131 ± 21 μM, respectively). As compared to control, in situ mitochondria in transgenic ventricular and slow-twitch muscles showed two times lower Km values for ADP, and the presence of creatine only slightly decreased the Km values. In mutant fast-twitch muscle, a decrease rather than increase in mitochondrial sensitivity to ADP occurred, but creatine still had no effect. Furthermore, in these muscles, relatively low oxidative capacity was considerably elevated. It is suggested that in the mutant mice, impairment of energy transport function in ventricular and slow-twitch muscles is compensated by a facilitation of adenine nucleotide transportation between mitochondria and cellular ATPases; in fast-twitch muscle, mainly energy buffering function is depressed, and that is overcome by an increase in energy-producing potential.
AB - Functional properties of in situ mitochondria and of mitochondrial creatine kinase were studied in saponin-skinned fibers taken from normal and M-creatine kinase-deficient mice. In control animals, apparent Km values of mitochondrial respiration for ADP in cardiac (ventricular) and slow-twitch (soleus) muscles (137 ± 16 μM and 209 ± 10 μM, respectively) were manyfold higher than that in fast-twitch (gastrocnemius) muscle (7.5 ± 0.5 μM). Creatine substantially decreased the Km values only in cardiac and slow-twitch muscles (73 ± 11 μM and 131 ± 21 μM, respectively). As compared to control, in situ mitochondria in transgenic ventricular and slow-twitch muscles showed two times lower Km values for ADP, and the presence of creatine only slightly decreased the Km values. In mutant fast-twitch muscle, a decrease rather than increase in mitochondrial sensitivity to ADP occurred, but creatine still had no effect. Furthermore, in these muscles, relatively low oxidative capacity was considerably elevated. It is suggested that in the mutant mice, impairment of energy transport function in ventricular and slow-twitch muscles is compensated by a facilitation of adenine nucleotide transportation between mitochondria and cellular ATPases; in fast-twitch muscle, mainly energy buffering function is depressed, and that is overcome by an increase in energy-producing potential.
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M3 - Article
C2 - 7650007
AN - SCOPUS:0029147509
SN - 0021-9258
VL - 270
SP - 19921
EP - 19929
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
IS - 34
ER -