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首页> 外文期刊>Life sciences >Casted-immobilization downregulates glucocorticoid receptor expression in rat slow-twitch soleus muscle.
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Casted-immobilization downregulates glucocorticoid receptor expression in rat slow-twitch soleus muscle.

机译：铸造固定化下调糖皮质激素受体表达在大鼠慢速抽搐Soleus肌肉中。

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AIMS: Glucocorticoids bind to the glucocorticoid receptor (GR) and increase catabolism of muscle proteins via the ubiquitin-proteasome pathway. Activation of beta(2)-adrenergic receptor (beta(2)-AR) in skeletal muscle has been shown to induce muscle hypertrophy by promoting muscle protein synthesis and/or attenuating protein degradation. The aim of this study was to investigate the correlation between disuse-induced muscle atrophy, and expression of GR and beta(2)-AR. METHODS: Rats were subjected to casted-immobilization (knee and foot arthrodesis), a model for muscle disuse, for 10 days. Fast-twitch (extensor digitorum longus: EDL) and slow-twitch (soleus: SOL) muscles were isolated and subsequently used for analysis. The expression of GR and beta(2)-AR was analyzed by real-time RT-PCR and western blotting. In addition, we analyzed plasma catecholamine and corticosterone concentrations by ELISA. KEY FINDINGS: Casted-immobilization-induced muscle atrophy was much greater in the SOL muscle than in the EDL muscle. Casted-immobilization decreased the expression of GR mRNA and protein in the SOL muscle but not in the EDL muscle. Although the expression of beta(2)-AR protein in the cytosol and membrane-rich fractions was not changed by casted-immobilization in either muscle, casted-immobilization decreased the expression of beta(2)-AR mRNA in the SOL muscle. Plasma catecholamine and corticosterone concentrations, however, were largely unaffected by casted-immobilization during the experimental period. SIGNIFICANCE: This study provides evidence that casted-immobilization-induced muscle disuse downregulates GR expression in slow-twitch muscle. These results suggest that muscle disuse suppresses glucocorticoid signals, such as muscle protein breakdown and transcription of the beta(2)-AR gene, via downregulation of GR expression in slow-twitch muscle.
机译：目的：糖皮质激素与糖皮质激素受体（GR）结合，并通过遍突蛋白蛋白酶体途径增加肌肉蛋白的分解代谢。已经显示骨骼肌中β（2） - 肾上腺素能受体（β（2）-AR）通过促进肌肉蛋白质合成和/或衰减蛋白质降解来诱导肌肉肥大。本研究的目的是探讨废弃诱导的肌肉萎缩与GR和β（2）-AR的表达之间的相关性。方法：对大鼠进行浇铸固定化（膝关节节动力），肌肉剥离模型10天。分离出快速抽搐（伸展位数：EDL）和慢速（SOLEUS：SOL）肌肉，随后用于分析。通过实时RT-PCR和Western印迹分析GR和Beta（2）-AR的表达。此外，我们通过ELISA分析了血浆儿茶酚胺和皮质酮浓度。主要发现：铸造 - 固定诱导的肌肉萎缩在肌肉肌肉中比EDL肌肉更大。铸造 - 固定化降低了溶胶肌肉中GR mRNA和蛋白的表达，但不在EDL肌肉中。尽管在任何肌肉中，β（2） - 富含型富含细胞溶胶和富含膜的级分中的蛋白质的表达不会在肌肉中的浇铸固定化，铸造 - 固定化降低了溶胶肌肉中β（2）-AR mRNA的表达。然而，血浆儿茶酚胺和皮质酮浓度在实验期间通过浇铸固定化的主要不受影响。意义：本研究提供了证据，即铸造 - 固定诱导的肌肉废物在缓慢抽搐肌肉中下调GR表达。这些结果表明，肌肉废弃抑制糖皮质激素信号，例如肌肉蛋白崩溃和β（2）-AR基因的转录，通过下调在缓慢抽搐肌肉中的r GR表达。

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