The effect of muscle length on post-tetanic potentiation of C57BL/6 and skMLCK-/- mouse EDL muscles.

IF 1.8 3区 生物学 Q4 CELL BIOLOGY
Angelos Angelidis, Rene Vandenboom
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引用次数: 0

Abstract

Post-tetanic potentiation of fast-twitch skeletal muscle is dependent on muscle length, with greater potentiation observed at shorter compared to longer lengths. The structural effects of the primary potentiation mechanism, phosphorylation of the regulatory light chain (RLC) of myosin, are thought to explain this relationship. The purpose of these experiments was to determine whether the length-dependence of potentiation would be attenuated in the absence of RLC phosphorylation. To this end, we compared isometric twitch potentiation of mouse extensor digitorum longus (EDL) muscles with (wildtype, WT) and without (skeletal myosin light chain kinase knockout, skMLCK-/-) phosphorylation. Force was measured at five muscle lengths (0.90 Lo, 0.95 Lo, Lo, 1.05 Lo, 1.10 Lo, where Lo refers to optimal length) prior to and following a tetanic train. In accordance with prior findings, potentiation was dependent on muscle length, with greater values observed at short (e.g., 44.3 ± 4.6% for WT, 33.5 ± 6.2% for skMLCK-/-, at 0.90 Lo) compared to long lengths (e.g., 16.9 ± 1.3% for WT, 9.1 ± 1.8% for skMLCK-/-, at 1.10 Lo) in both genotypes. WT muscles displayed greater potentiation compared to their skMLCK-/- counterparts across lengths (e.g., 16.9 ± 1.6% vs 7.3 ± 1.5% at Lo). However, the relationship between potentiation and muscle length was not different between genotypes. Thus, the alternative mechanisms of potentiation, present in the skMLCK-/- EDL, display a length-dependence of post-tetanic potentiation similar to RLC phosphorylation-dominant potentiation. Additional mechanisms may be required to explain the length-dependence of potentiation.

Abstract Image

肌肉长度对C57BL/6和skMLCK-/-小鼠EDL肌肉破伤风后增强的影响。
破伤风后快速抽搐骨骼肌的增强依赖于肌肉长度,较短的肌肉比较长的肌肉有更大的增强。主要增强机制的结构效应,肌球蛋白的调控轻链(RLC)的磷酸化,被认为可以解释这种关系。这些实验的目的是确定在没有RLC磷酸化的情况下,增强的长度依赖性是否会减弱。为此,我们比较了(野生型,WT)和未(骨骼肌蛋白轻链激酶敲除,skMLCK-/-)磷酸化的小鼠指长伸肌(EDL)肌肉的等距抽搐增强。在强直性训练之前和之后测量五种肌肉长度(0.90 Lo, 0.95 Lo, Lo, 1.05 Lo, 1.10 Lo,其中Lo指最佳长度)的力。根据先前的研究结果,增强作用依赖于肌肉长度,在两种基因型中,与长长度(例如,WT为44.3±4.6%,skMLCK-/-为33.5±6.2%,0.90 Lo)相比,短长度的值更大(例如,WT为16.9±1.3%,skMLCK-/-为9.1±1.8%,1.10 Lo)。与skMLCK-/-相比,WT肌肉在不同长度上表现出更大的增强(例如,在Lo时为16.9±1.6% vs 7.3±1.5%)。然而,增强与肌肉长度的关系在不同基因型之间没有差异。因此,skMLCK-/- EDL中存在的另一种增强机制显示出破伤风后增强的长度依赖性,类似于RLC磷酸化显性增强。可能需要其他机制来解释增强作用的长度依赖性。
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来源期刊
CiteScore
6.20
自引率
0.00%
发文量
21
审稿时长
>12 weeks
期刊介绍: The Journal of Muscle Research and Cell Motility has as its main aim the publication of original research which bears on either the excitation and contraction of muscle, the analysis of any one of the processes involved therein, the processes underlying contractility and motility of animal and plant cells, the toxicology and pharmacology related to contractility, or the formation, dynamics and turnover of contractile structures in muscle and non-muscle cells. Studies describing the impact of pathogenic mutations in genes encoding components of contractile structures in humans or animals are welcome, provided they offer mechanistic insight into the disease process or the underlying gene function. The policy of the Journal is to encourage any form of novel practical study whatever its specialist interest, as long as it falls within this broad field. Theoretical essays are welcome provided that they are concise and suggest practical ways in which they may be tested. Manuscripts reporting new mutations in known disease genes without validation and mechanistic insight will not be considered. It is the policy of the journal that cells lines, hybridomas and DNA clones should be made available by the developers to any qualified investigator. Submission of a manuscript for publication constitutes an agreement of the authors to abide by this principle.
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