Irisin prevents dexamethasone-induced atrophy in C2C12 myotubes

Jae Seung Chang, In Deok Kong

Research output: Contribution to journalArticlepeer-review

Abstract

Irisin is a myokine secreted mainly from skeletal muscle that is known for having beneficial metabolic effects via enhancement of energy expenditure and insulin sensitivity. Studies show that irisin also acts as an autocrine/paracrine to promote myogenesis and muscle growth. However, the protective role of irisin against muscular wasting remains unclear. We confirmed that irisin secretion was upregulated by electrical pulse stimulation an in vitro exercise mimetic model. Next, we tested if irisin exerted an anti-atrophic effect on cultured C2C12 myotubes treated with dexamethasone (DEX), a representative inducer of muscular atrophy. Treatment of cultured myotubes with DEX reduced myotube size and increased proteasome activity, which were attenuated by irisin. Also, irisin effectively prevented dephosphorylation of forkhead box O (FoxO) 3α and upregulation of muscle-specific ubiquitin ligases in DEX-treated myotubes. The protective effect of irisin on DEX-mediated myotube atrophy was partially regulated by insulin-like growth factor-1-dependent signaling. These results suggested that irisin may prevent glucocorticoid-induced muscle atrophy by inhibiting FoxO-mediated ubiquitin-proteasome overactivity.

Original languageEnglish
Pages (from-to)495-502
Number of pages8
JournalPflugers Archiv European Journal of Physiology
Volume472
Issue number4
DOIs
Publication statusPublished - 2020 Apr 1

Bibliographical note

Funding Information:
This study was supported by the National Research Foundation of Korea grant funded by the Korea government (NRF-2018R1C1B6005036 and NRF-2017R1A5A2015369) and in part by the Yonsei University Research Fund of 2018.

All Science Journal Classification (ASJC) codes

  • Physiology
  • Clinical Biochemistry
  • Physiology (medical)

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