Changes in glycolytic network and mitochondrial design in creatine kinase-deficient muscles
Changes in glycolytic network and mitochondrial design in creatine kinase-deficient muscles
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DOI：
10.1002/mus.1131
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发表时间：
2001-09-01
期刊：
影响因子：
3.4
通讯作者：
Wieringa, B
中科院分区：
文献类型：
--
作者：
de Groof, AJC;Oerlemans, FTJJ;Wieringa, B
骨骼肌通过重塑单个肌细胞的细胞结构和代谢特征，对病理生物学条件或生理需求的变化具有高度可塑性。我们以前已经表明，没有线粒体和/或胞质肌酸激酶（ScCKmit（-/-）和/或M-CK-/-）的小鼠肌肉通过重定向代谢途径和超微结构特征部分补偿缺陷。在这里，我们通过半定量蛋白质印迹分析表明，补偿性变化涉及突变和纤维类型特异性协调调节不同但功能耦合的蛋白质组。CK-/-小鼠的快缩腓肠肌显示线粒体细胞色素c氧化酶、无机磷酸载体、腺嘌呤核苷酸转运体和电压依赖性阴离子通道蛋白的2 - 4倍上调。同时，胞浆肌红蛋白上调。慢收缩比目鱼肌的反应是糖酵解酶模式的变化，包括乳酸脱氢酶同工酶组成的变化。在17日龄时，氧化三磷酸腺苷（ATP）产生的网络适应已经很明显。(C)John Wiley & Sons，Inc.
Skeletal muscles respond with high plasticity to pathobiological conditions or changes in physiological demand by remodeling cytoarchitectural and metabolic characteristics of individual myocytes. We have previously shown that muscles of mice without mitochondrial and/or cytosolic creatine kinases (ScCKmit(-/-) and/or M-CK-/-) partly compensate for the defect(s) by redirecting metabolic pathways and ultrastructural characteristics. Here, we show by semiquantitative Western blot analysis that the compensatory changes involve mutation- and fiber-type-specific coordinated regulation of divergent but functionally coupled groups of proteins. Fast-twitch gastrocnemius muscle of CK-/- mice display a two- to fourfold upregulation of mitochondrial cytochrome c oxidase, inorganic phosphate carrier, adenine nucleotide translocator, and voltage-dependent anion channel proteins. In parallel, cytosolic myoglobin is upregulated. Slow-twitch soleus muscle responds with changes in the glycolytic enzyme pattern, including a shift in lactate dehydrogenase isoenzyme composition. Adaptations in the network for oxidative adenosine triphosphate (ATP) production are already apparent at 17 days of age. (C) 2001 John Wiley & Sons, Inc.