highlighted topics Plasticity in Skeletal, Cardiac, and Smooth Muscle Invited Review: Effects of different activity and inactivity paradigms on myosin heavy chain gene expression in striated muscle
highlighted topics Plasticity in Skeletal, Cardiac, and Smooth Muscle Invited Review: Effects of different activity and inactivity paradigms on myosin heavy chain gene expression in striated muscle
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发表时间：
2000
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通讯作者：
K. M. Baldwin;F. Haddad
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作者：
K. M. Baldwin;F. Haddad
特邀评论：不同活动和不活动模式对横纹肌肌球蛋白重链基因表达的影响。J Appl Physiol 90：345 - 357，2001. -这篇小型综述的目的是总结关于肌肉活动和不活动的不同模型在改变哺乳动物心脏和骨骼肌中肌球蛋白重链（MHC）家族运动蛋白基因表达中所起作用的发现。这是在检查甲状腺激素（T3，3，5，3 9-三碘甲状腺原氨酸）在MHC表达中所起作用的平行发现的背景下进行的。研究结果表明，实验动物的心肌和骨骼肌在出生时均未分化，然后经历显著的生长和分化，以T3/活性水平依赖的方式获得成年MHC表型。小型哺乳动物的心脏MHC表达对甲状腺功能低下、糖尿病、能量缺乏和高血压高度敏感;这些干预措施中的每一种都诱导B-MHC亚型的上调，其功能是在能量需求改变时节约循环功能。在骨骼肌中，甲状腺功能亢进症，以及卸载或减少肌肉承重活动的干预措施，导致慢到快的MHC转换。然而，在甲状腺功能减退症或肌肉长期超负荷或在阻力训练和耐力运动期间受到间歇性负荷时，可以看到快速到缓慢的转换。根据最近对转基因模型和用启动子-报告基因结构转染的动物的发现，T3或机械刺激对MHC基因表达的调节似乎受到转录事件的强烈调节。然而，T3和机械刺激对转录过程的控制机制似乎是不同的。额外的发现表明，单个骨骼肌纤维具有同时表达所有成人MHC的遗传机制，例如，慢I型和快IIa，IIx和IIb，在某些实验条件下的独特组合。个体纤维之间这种程度的异质性将确保在执行复杂运动模式时具有很大的功能多样性。未来的研究必须集中在1）信号通路和控制这种显著可塑性程度的转录/翻译机制的潜在机制，以及2）肌肉纤维表达这种多样性运动蛋白的能力的形态组织和功能意义。
Invited Review: Effects of different activity and inactivity paradigms on myosin heavy chain gene expression in striated muscle. J Appl Physiol 90: 345–357, 2001.—The goal of this mini-review is to summarize findings concerning the role that different models of muscular activity and inactivity play in altering gene expression of the myosin heavy chain (MHC) family of motor proteins in mammalian cardiac and skeletal muscle. This was done in the context of examining parallel findings concerning the role that thyroid hormone (T 3 , 3,5,3 9 -triiodothyronine) plays in MHC expres- sion. Findings show that both cardiac and skeletal muscles of experimental animals are initially undifferentiated at birth and then undergo a marked level of growth and differentiation in attaining the adult MHC phenotype in a T 3 /activity level-dependent fashion. Cardiac MHC ex- pression in small mammals is highly sensitive to thyroid deficiency, diabetes, energy deprivation, and hypertension; each of these interventions induces upregulation of the b -MHC isoform, which functions to economize circulatory function in the face of altered energy demand. In skeletal muscle, hyperthyroidism, as well as interventions that unload or reduce the weight-bearing activity of the muscle, causes slow to fast MHC conversions. Fast to slow conversions, however, are seen under hypothyroidism or when the muscles either become chronically overloaded or subjected to intermittent loading as occurs during resistance training and endurance exercise. The regulation of MHC gene expression by T 3 or mechanical stimuli appears to be strongly regulated by tran- scriptional events, based on recent findings on transgenic models and animals transfected with promoter-reporter constructs. However, the mechanisms by which T 3 and mechanical stimuli exert their control on transcriptional processes appear to be different. Additional findings show that individual skeletal muscle fibers have the genetic machinery to express simultaneously all of the adult MHCs, e.g., slow type I and fast IIa, IIx, and IIb, in unique combinations under certain experimental conditions. This degree of heterogeneity among the individual fibers would ensure a large functional diversity in performing complex movement patterns. Future studies must now focus on 1 ) the signaling pathways and the underlying mechanisms governing the transcriptional/ translational machinery that control this marked degree of plasticity and 2 ) the morphological organization and functional implications of the muscle fiber’s capacity to express such a diversity of motor proteins.