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Loading‐associated expression of TRIM72 and caveolin‐3 in antigravitational soleus muscle in mice

机译:小鼠抗重力比目鱼肌中TRIM72和小窝蛋白3的负荷相关表达

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摘要

Effects of mechanical loading on the expression level of tripartite motif‐containing 72 (TRIM72) and caveolin‐3 (Cav‐3) in mouse soleus muscle were investigated. Mice were subjected to (1) continuous hindlimb suspension (HS) for 2 weeks followed by 1‐week ambulation recovery or (2) functional overloading (FO) on the soleus by cutting the distal tendons of the plantaris and gastrocnemius muscles. Soleus muscle atrophy was induced by 2‐week hindlimb suspension (HS). Reloading‐associated regrowth of atrophied soleus muscle was observed by 1‐week reloading following HS. HS also depressed the expression level of insulin receptor substrate‐1 (IRS‐1) mRNA, TRIM72, Cav‐3, and phosphorylated Akt (p‐Akt)/total Akt (t‐Akt), but increased the phosphorylated level of p38 mitogen‐activated protein kinase (p‐p38MAPK) in soleus muscle. Thereafter, the expression level of MyoD mRNA, TRIM72 (mRNA, and protein), and Cav‐3 was significantly increased and recovered to the basal level during 1‐week reloading after HS. Although IRS‐1 expression was also upregulated by reloading, the expression level was significantly lower than that before HS. Significant increase in p‐Akt and phosphorylated p70 S6 kinase (p‐p70S6K) was observed by 1‐day reloading. On the other hand, 1‐week functional overloading (FO) induced soleus muscle hypertrophy. In FO‐associated hypertrophied soleus muscle, the expression level of IRS‐1 mRNA, MyoD mRNA, TRIM72 mRNA, p‐Akt, and p‐p70S6K was increased, but the expression of Cav‐3 and p‐p38MAPK was decreased. FO had no effect on the protein expression level of TRIM72. These observations suggest that the loading‐associated upregulation of TRIM72 protein in skeletal muscle may depress the regrowth of atrophied muscle via a partial suppression of IRS‐1. In addition, downregulation of Cav‐3 in skeletal muscle may depress overloading‐induced muscle hypertrophy.
机译:研究了机械负荷对小鼠比目鱼肌中含三方基序72(TRIM72)和小窝蛋白3(Cav-3)表达水平的影响。对小鼠进行(1)连续后肢悬吊(HS)2周,然后进行1周的步行运动恢复,或(2)通过切开足底和腓肠肌远侧肌腱使比目鱼肌功能超负荷(FO)。比目鱼肌萎缩是由2周后肢悬吊(HS)引起的。在HS后1周的再负荷可以观察到与萎缩的比目鱼肌再负荷相关的再生。 HS还抑制了胰岛素受体底物-1(IRS-1)mRNA,TRIM72,Cav-3和磷酸化Akt(p-Akt)/总Akt(t-Akt)的表达水平,但增加了p38促分裂原的磷酸化水平比目鱼肌中激活的蛋白激酶(p-p38MAPK)。此后,在HS后1周重载期间,MyoD mRNA,TRIM72(mRNA和蛋白)和Cav-3的表达水平显着增加并恢复至基础水平。尽管IRS-1表达也因重载而上调,但表达水平明显低于HS之前。在第1天重新加载后,观察到p-Akt和磷酸化的p70 S6激酶(p-p70S6K)显着增加。另一方面,1周的功能性超负荷(FO)导致比目鱼肌肥大。在与FO相关的肥大比目鱼肌中,IRS-1 mRNA,MyoD mRNA,TRIM72 mRNA,p‐Akt和p‐p70S6K的表达水平增加,但Cav‐3和p‐p38MAPK的表达减少。 FO对TRIM72的蛋白表达水平没有影响。这些观察结果表明骨骼肌中TRIM72蛋白的负荷相关上调可能通过部分抑制IRS-1来抑制萎缩性肌肉的再生。此外,骨骼肌中Cav-3的下调可能会抑制超负荷引起的肌肉肥大。

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