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首页> 外文期刊>Journal of Cachexia, Sarcopenia and Muscle >The delayed recovery of the remobilized rat tibialis anterior muscle reflects a defect in proliferative and terminal differentiation that impairs early regenerative processes
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The delayed recovery of the remobilized rat tibialis anterior muscle reflects a defect in proliferative and terminal differentiation that impairs early regenerative processes

机译：动员的大鼠胫骨前肌的恢复延迟反映出增殖和终末分化的缺陷，损害了早期的再生过程

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AbstractBackgroundThe immobilization-induced tibialis anterior (TA) muscle atrophy worsens after cast removal and is associated with altered extracellular matrix (ECM) composition. The secreted protein acidic and rich in cysteine (Sparc) is an ECM component involved in Akt activation and in β-catenin stabilization, which controls protein turnover and induces muscle regulatory factors (MRFs), respectively. We hypothesized that ECM alterations may influence these intracellular signalling pathways controlling TA muscle mass.MethodsSix-month-old Wistar rats were subjected to hindlimb cast immobilization for 8 days (I8) or not (I0) and allowed to recover for 1 to 10 days (R1–10).ResultsThe TA atrophy during remobilization correlated with reduced fibre cross-sectional area and thickening of endomysium. mRNA levels for Sparc increased during remobilization until R10 and for integrin-α7 and -β1 at I8 and R1. Integrin-linked kinase protein levels increased during immobilization and remobilization until R10. This was inversely correlated with changes in Akt phosphorylation. β-Catenin protein levels increased in the remobilized TA at R1 and R10. mRNA levels of the proliferative MRFs (Myf5 and MyoD) increased at I8 and R1, respectively, without changes in Myf5 protein levels. In contrast, myogenin mRNA levels (a terminal differentiation MRF) decreased at R1, but only increased at R10 in remobilized muscles, as for protein levels.ConclusionsAltogether, this suggests that the TA inefficiently attempted to preserve regeneration during immobilization by increasing transcription of proliferative MRFs, and that the TA could engage recovery during remobilization only when the terminal differentiation step of regeneration is enhanced.
机译：摘要背景固定化引起的胫前肌（TA）肌肉萎缩在脱模后恶化，并且与改变的细胞外基质（ECM）成分有关。分泌的酸性蛋白和富含半胱氨酸（Sparc）是一种ECM成分，参与Akt激活和β-catenin稳定，分别控制蛋白质更新并诱导肌肉调节因子（MRF）。我们假设ECM改变可能会影响这些控制TA肌肉质量的细胞内信号传导途径。方法对6个月大的Wistar大鼠进行后肢石膏固定8天（I8）或不固定（I0），使其恢复1至10天（ R1-10）。结果复律期间TA萎缩与纤维横截面积减少和内膜增厚有关。 Sparc的mRNA水平在运输过程中一直升高，直到R10为止，而在I8和R1处的整联蛋白-α7和-β1则升高。整联蛋白连接的激酶蛋白水平在固定和固定过程中增加，直到R10。这与Akt磷酸化的变化呈负相关。 R1和R10处重新固定的TA中的β-Catenin蛋白水平增加。增生性MRF（Myf5和MyoD）的mRNA水平在I8和R1分别升高，而Myf5蛋白水平没有变化。相比之下，就蛋白质水平而言，肌动蛋白的mRNA水平（终末分化MRF）在R1处降低，但在R10处仅升高（在蛋白质水平上）。结论综上所述，这提示TA在固定化过程中低效率地尝试通过增加增殖性MRF的转录来保持再生。 ，并且只有在再生的终末分化步骤得到增强时，TA才能在复员期间参与恢复。

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