Hoffman R K, Gambke B, Stephenson L W, Rubinstein N A
Muscle Nerve. 1985 Nov-Dec;8(9):796-805. doi: 10.1002/mus.880080909.
Chronic low-frequency stimulation of a fast skeletal muscle effects a transition of myosin isozymes from those characteristic of a fast muscle to those characteristic of a slow muscle. This transformation involves changes in both myosin heavy and light chains. During development, muscles usually change directly from embryonic to neonatal to fast or from embryonic to neonatal to slow isozymes. We have questioned whether chronic stimulation of the adult fast muscle results in a direct fast-to-slow isozyme shift or whether transformation requires reexpression of the developmental isozymes prior to the synthesis of adult slow isozymes. We have examined these alternatives in the chronically stimulated dog diaphragm using adenosine triphosphatase (ATPase) histochemistry, pyrophosphate gel electrophoresis of native isozymes, peptide mapping of myosin heavy chains, immunoblotting with an antibody specific to embryonic myosin heavy chain, and solid-phase radioimmunoassay. We have demonstrated that a transition from adult fast to adult slow isozymes during chronic stimulation does not involve a recapitulation of embryonic isozymes.
对快速骨骼肌进行慢性低频刺激会使肌球蛋白同工酶从快速肌肉特有的同工酶转变为慢速肌肉特有的同工酶。这种转变涉及肌球蛋白重链和轻链的变化。在发育过程中，肌肉通常直接从胚胎型转变为新生型，再转变为快速型同工酶或从胚胎型转变为新生型，再转变为慢速型同工酶。我们曾质疑，对成年快速肌肉进行慢性刺激是否会导致直接的快速型到慢速型同工酶转变，或者这种转变是否需要在合成成年慢速同工酶之前重新表达发育中的同工酶。我们使用三磷酸腺苷酶（ATPase）组织化学、天然同工酶的焦磷酸凝胶电泳、肌球蛋白重链的肽图谱分析、用针对胚胎肌球蛋白重链的特异性抗体进行免疫印迹以及固相放射免疫测定法，在慢性刺激的犬膈肌中研究了这些可能性。我们已经证明，在慢性刺激过程中从成年快速型同工酶到成年慢速型同工酶的转变并不涉及胚胎同工酶的重现。
