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首页> 外文期刊>Skeletal Muscle >Transgenic overexpression of γ-cytoplasmic actin protects against eccentric contraction-induced force loss in mdx mice
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Transgenic overexpression of γ-cytoplasmic actin protects against eccentric contraction-induced force loss in mdx mice

机译：γ-胞质肌动蛋白的转基因过表达可防止mdx小鼠因离心收缩引起的力损失

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Background γ-cytoplasmic (γ-cyto) actin levels are elevated in dystrophin-deficient mdx mouse skeletal muscle. The purpose of this study was to determine whether further elevation of γ-cyto actin levels improve or exacerbate the dystrophic phenotype of mdx mice. Methods We transgenically overexpressed γ-cyto actin, specifically in skeletal muscle of mdx mice (mdx-TG), and compared skeletal muscle pathology and force-generating capacity between mdx and mdx-TG mice at different ages. We investigated the mechanism by which γ-cyto actin provides protection from force loss by studying the role of calcium channels and stretch-activated channels in isolated skeletal muscles and muscle fibers. Analysis of variance or independent t-tests were used to detect statistical differences between groups. Results Levels of γ-cyto actin in mdx-TG skeletal muscle were elevated 200-fold compared to mdx skeletal muscle and incorporated into thin filaments. Overexpression of γ-cyto actin had little effect on most parameters of mdx muscle pathology. However, γ-cyto actin provided statistically significant protection against force loss during eccentric contractions. Store-operated calcium entry across the sarcolemma did not differ between mdx fibers compared to wild-type fibers. Additionally, the omission of extracellular calcium or the addition of streptomycin to block stretch-activated channels did not improve the force-generating capacity of isolated extensor digitorum longus muscles from mdx mice during eccentric contractions. Conclusions The data presented in this study indicate that upregulation of γ-cyto actin in dystrophic skeletal muscle can attenuate force loss during eccentric contractions and that the mechanism is independent of activation of stretch-activated channels and the accumulation of extracellular calcium.
机译：在肌营养不良蛋白缺陷的mdx小鼠骨骼肌中，背景γ胞质（γ-细胞）肌动蛋白水平升高。这项研究的目的是确定γ细胞肌动蛋白水平的进一步提高是否改善或加剧了mdx小鼠的营养不良表型。方法我们转基因过度表达了γ-细胞肌动蛋白，特别是在mdx小鼠（mdx-TG）的骨骼肌中，并比较了不同年龄的mdx和mdx-TG小鼠的骨骼肌病理学和力量产生能力。我们通过研究钙通道和拉伸激活通道在孤立的骨骼肌和肌肉纤维中的作用，研究了γ-细胞肌动蛋白提供保护免受力损失的机制。方差分析或独立t检验用于检测组之间的统计差异。结果与mdx骨骼肌相比，mdx-TG骨骼肌中的γ-细胞肌动蛋白水平提高了200倍，并掺入细丝中。 γ-细胞肌动蛋白的过表达对mdx肌肉病理的大多数参数影响很小。但是，γ-细胞肌动蛋白在偏心收缩过程中提供了统计学上显着的防止力损失的保护作用。与野生型纤维相比，mdx纤维之间通过肌膜存储的钙操作没有差异。另外，省略细胞外钙或添加链霉素以阻断拉伸激活的通道并不能改善在离心收缩过程中从mdx小鼠分离出的指伸长肌的力量产生能力。结论本研究提供的数据表明，营养不良性骨骼肌中γ-细胞肌动蛋白的上调可以减弱离心收缩过程中的力损失，并且该机制与拉伸激活通道的激活和细胞外钙的积累无关。

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