Changes in Ca2+ handling in adult MG29-deficient skeletal muscle
Changes in Ca2+ handling in adult MG29-deficient skeletal muscle
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DOI：
10.1016/j.bbrc.2003.09.146
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发表时间：
2003-10-31
影响因子：
3.1
通讯作者：
Ogawa, Y
中科院分区：
文献类型：
--
作者：
Kurebayashi, N;Takeshima, H;Ogawa, Y
据报道，缺乏Mitsugumin29 (MG29)，一种表达于三联体的蛋白，会导致肌浆网和t小管的形态学改变，降低抽搐/破伤风比，增加成人骨骼肌的疲劳易感，以及胚胎和新生儿肌肉的储存操作Ca2+进入（SOC）功能障碍。为了加深我们对MG29在成人骨骼肌Ca2+处理中的作用的理解，野生型和突变型肌纤维的Ca2+储存通过在无Ca2+培养基中重复高k +处理而耗尽。尽管野生型肌肉在高k +反应消失后仅表现出轻微的咖啡因挛缩，但在使用的条件下，突变肌肉表现出显著的咖啡因挛缩，这表明突变体中Ca2+储存的功能区隔化。与野生型肌肉一样，在电压敏感型肌肉中观察到成年突变肌肉中SOC的激活。因此，MG29不参与未成熟肌肉的SOC激活，这与之前的结论不同。(C) 2003 Elsevier Inc.版权所有。
It was reported that a lack of Mitsugumin29 (MG29), a protein expressed at the triad junction, caused morphological changes in sarcoplasmic reticulum and T-tubules, reduced twitch/tetanus ratio, and increased susceptibility to fatigue in adult skeletal muscle and dysfunction of store-operated Ca2+ entry (SOC) in embryonic and neonatal muscles. To deepen our understanding of the role of MG29 in the Ca2+ handling in adult skeletal muscle, Ca2+ stores of wild-type and mutant muscle fibers were depleted by repetitive high-K+ treatments in a Ca2+-free medium. Although wild-type muscle showed only minor caffeine contracture after high-K+ response had disappeared, the mutant muscle showed remarkable caffeine contracture under the conditions used, suggesting functional compartmentalization of the Ca2+-store in the mutant. Activation of SOC in adult mutant muscle was observed upon the voltage-sensitive store depletion as is true with the wild-type muscle. Thus MG29 is not involved in the SOC activation at variance with the previous conclusion with immature muscles. (C) 2003 Elsevier Inc. All rights reserved.