Metabolic Suppression by 3-Iodothyronamine Induced Muscle Cell Atrophy <i>via</i> Activation of FoxO–Proteasome Signaling and Downregulation of Akt1–S6K Signaling

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<p>The homeostasis of muscle properties depends on both physical and metabolic stresses. Whereas physical stress entails metabolic response for muscle homeostasis, the latter does not necessarily involve the former and may thus solely affect the homeostasis. We here report that metabolic suppression by the hypometabolic agent 3-iodothyronamine (T1AM) induced muscle cell atrophy without physical stress. We observed that the oxygen consumption rate of C2C12 myotubes decreased 40% upon treatment with 75 µM T1AM for 6 h <i>versus</i> 10% in the vehicle (dimethyl sulfoxide) control. The T1AM treatment reduced cell diameter of myotubes by 15% compared to the control (<i>p</i><0.05). The cell diameter was reversed completely by 9 h after T1AM was removed. The T1AM treatment also significantly suppressed the expression levels of heat shock protein 72 and αB-crystallin as well as the phosphorylation levels of Akt1, mammalian target of rapamycin (mTOR), S6K, forkhead box O1 (FoxO1) and FoxO3. In contrast, the levels of ubiquitin E3 ligase MuRF1 and chymotrypsin-like activity of proteasome were significantly elevated by T1AM treatment. These results suggest that T1AM-mediated metabolic suppression induced muscle cell atrophy <i>via</i> activation of catabolic signaling and inhibition of anabolic signaling.</p>

収録刊行物

  • Biological & Pharmaceutical Bulletin

    Biological & Pharmaceutical Bulletin 40(5), 576-582, 2017

    公益社団法人 日本薬学会

各種コード

  • NII論文ID(NAID)
    130005631971
  • NII書誌ID(NCID)
    AA10885497
  • 本文言語コード
    ENG
  • ISSN
    0918-6158
  • NDL 記事登録ID
    028137479
  • NDL 請求記号
    Z53-V41
  • データ提供元
    NDL  J-STAGE 
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