Loading-associated expression of TRIM72 and caveolin-3 in antigravitational soleus muscle in mice.
Loading-associated expression of TRIM72 and caveolin-3 in antigravitational soleus muscle in mice.
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DOI：
10.14814/phy2.12259
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发表时间：
2014-12-01
影响因子：
2.5
通讯作者：
Goto K
中科院分区：
文献类型：
--
作者：
Ohno Y;Sugiura T;Ohira Y;Yoshioka T;Goto K
研究了机械负荷对小鼠比目鱼肌中含有三联基序 72 (TRIM72) 和小窝蛋白-3 (Cav-3) 表达水平的影响。对小鼠进行（1）持续后肢悬吊（HS）2周，然后进行1周的步行恢复或（2）通过切割跖肌和腓肠肌远端肌腱对比目鱼肌进行功能超载（FO）。两周后肢悬吊（HS）诱导比目鱼肌萎缩。通过 HS 后 1 周的重新加载观察到萎缩的比目鱼肌的重新加载相关的再生。 HS 还降低比目鱼肌中胰岛素受体底物 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 p38 丝裂原激活蛋白激酶 (p-p38MAPK) 的磷酸化水平。此后，MyoD mRNA、TRIM72（mRNA 和蛋白质）和 Cav-3 的表达水平显着增加，并在 HS 后 1 周的重新加载期间恢复至基础水平。虽然IRS-1表达也因重载而上调，但表达水平显着低于HS前。 1 天重新加载后观察到 p-Akt 和磷酸化 p70 S6 激酶 (p-p70S6K) 显着增加。另一方面，1周的功能超负荷（FO）会导致比目鱼肌肥大。在FO相关肥大的比目鱼肌中，IRS-1 mRNA、MyoD mRNA、TRIM72 mRNA、p-Akt和p-p70S6K的表达水平升高，但Cav-3和p-p38MAPK的表达水平降低。 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 蛋白与负荷相关的上调可能通过部分抑制 IRS-1 来抑制萎缩肌肉的再生。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。卸载后1周重装期间，MyoD和TRIM72的mRNA表达水平显着升高并恢复至基础水平。尽管重装后IRS-1表达也上调，但表达水平显着低于卸载前。骨骼肌中与负荷相关的 TRIM72 上调可能通过部分抑制 IRS-1 来抑制萎缩肌肉的再生。
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. The mRNA expression level of MyoD and TRIM72 was significantly increased and recovered to the basal level during 1‐week reloading after unloading. Although IRS‐1 expression was also upregulated by reloading, the expression level was significantly lower than that before unloading. The loading‐associated upregulation of TRIM72 in skeletal muscle may depress the regrowth of atrophied muscle via a partial suppression of IRS‐1.