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Cortisone and dexamethasone inhibit myogenesis by modulating the AKT/mTOR signaling pathway in C2C12

Jonggun Kim1, Min Young Park1, Hyung Kwan Kim1

  • 1a Department of Biotechnology , Korea University , Seoul , Republic of Korea.

Bioscience, Biotechnology, and Biochemistry
|July 22, 2016
PubMed

Insights

Therapeutic glucocorticoids like dexamethasone and cortisone suppress fetal myotube formation by disrupting myogenic regulatory factors and the IGF/PI3K/AKT/mTOR pathway, impacting muscle development.

Area of Science:

  • Muscle development and cellular biology
  • Endocrinology and pharmacology

Background:

  • Myogenesis, the process of muscle formation, occurs prenatally and postnatally, influencing long-term health.
  • Glucocorticoids are widely used therapeutics but can disrupt muscle homeostasis and fetal development.
  • While effects on differentiated muscle are known, glucocorticoid impact on myotube formation is less understood.

Purpose of the Study:

  • To investigate the effects of synthetic glucocorticoids, dexamethasone (DEX) and cortisone (COR), on myotube formation in vitro.
  • To elucidate the molecular mechanisms by which DEX and COR affect skeletal muscle development.

Main Methods:

  • Utilized C2C12 myoblast cell line for in vitro studies.
  • Assessed myotube formation and quantified changes in myogenic regulatory factors (MRFs).
  • Analyzed the IGF/PI3K/AKT/mTOR signaling pathway and protein metabolism markers.

Main Results:

  • Dexamethasone (DEX) and cortisone (COR) significantly suppressed myotube formation in C2C12 cells.
  • Both glucocorticoids modulated the expression of myogenic regulatory factors (MRFs).
  • DEX and COR altered the IGF/PI3K/AKT/mTOR pathway, increasing muscle degradation proteins (atrogin-1, MURF1) and decreasing ribosomal S6 phosphorylation.

Conclusions:

  • Synthetic glucocorticoids DEX and COR inhibit myotube formation in C2C12 cells.
  • This inhibition occurs via modulation of the myogenic program through MRFs.
  • Glucocorticoids also impact protein metabolism via the IGF/PI3K/AKT/mTOR signaling pathway, contributing to muscle degradation.
Keywords:
C2C12cortisonedexamethasoneglucocorticoidmyogenesis

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