Inhibition of Sesn2 has negative regulatory effects on the myogenic differentiation of C2C12 myoblasts

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Updated: Jul 10, 2026

Modeling Myotonic Dystrophy 1 in C2C12 Myoblast Cells
09:39

Modeling Myotonic Dystrophy 1 in C2C12 Myoblast Cells

Published on: July 29, 2016

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Zubiao Song1, Qing Lin1, Jiahui Liang1

  • 1Department of Neurology, The First Affiliated Hospital, Sun Yat-Sen University; Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases; National Key Clinical Department and Key Discipline of Neurology, No. 58 Zhongshan Road 2, Guangzhou, 510080, China.

Molecular Biomedicine
|August 8, 2024
PubMed

Insights

Sestrin2 (Sesn2) promotes muscle cell differentiation and regeneration. MicroRNA-182-5p represses Sesn2, hindering myogenesis, suggesting therapeutic potential for muscular dystrophy.

Area of Science:

  • Muscle biology
  • Molecular genetics
  • Cellular stress response

Background:

  • Sestrin2 (Sesn2) is a known stress-response protein.
  • The role of Sesn2 in muscle cell differentiation (myogenesis) is not well understood.
  • Duchenne muscular dystrophy (DMD) is a severe genetic muscle-wasting disease.

Purpose of the Study:

  • To investigate the role of Sesn2 in C2C12 myoblast differentiation.
  • To explore the relationship between Sesn2 and microRNA-182-5p (miR-182-5p).
  • To examine Sesn2's function in mdx mice, an animal model for DMD.

Main Methods:

  • Knockdown and overexpression of Sesn2 in C2C12 myoblasts.
  • Bioinformatic prediction and experimental validation of miR-182-5p targeting Sesn2.
  • Analysis of myogenic markers (Myogenin, Pax7) and myofiber type in mdx mice.

Main Results:

  • Sesn2 knockdown impaired C2C12 myoblast differentiation.
  • miR-182-5p was identified as a negative regulator of Sesn2, inhibiting myogenesis.
  • In mdx mice, Sesn2 modulation affected Myogenin and Pax7 expression and myofiber characteristics.

Conclusions:

  • Sesn2 plays a critical role in promoting myogenic differentiation and skeletal muscle regeneration.
  • miR-182-5p negatively regulates myogenesis by suppressing Sesn2.
  • Sesn2 represents a potential therapeutic target for treating muscular dystrophy.
Keywords:
Duchenne muscular dystrophyMyogenic differentiationSestrin2Slow-twitch myofibersmiR-182-5p

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