AMPK Phosphorylation Impacts Apoptosis in Differentiating Myoblasts Isolated from Atrophied Rat Soleus Muscle

Natalia A Vilchinskaya1, Sergey V Rozhkov1, Olga V Turtikova1

  • 1Myology Laboratory, Institute of Biomedical Problems RAS, 123007 Moscow, Russia.

Cells
|March 29, 2023
PubMed

Insights

AMP-activated protein kinase (AMPK) activation suppresses apoptosis in differentiating myoblasts from atrophied rat soleus muscle. Maintaining AMPK activity prevents increased cell death and maintains normal apoptotic marker expression during muscle atrophy.

Area of Science:

  • Muscle biology
  • Cellular and molecular physiology
  • Biochemistry

Background:

  • Muscle satellite cells (SCs) are crucial for myofiber regeneration.
  • Muscle atrophy is associated with reduced SC numbers due to apoptosis.
  • Decreased AMP-activated protein kinase (AMPK) activity in differentiating myoblasts from atrophied muscle suggests a link to apoptosis.

Purpose of the Study:

  • To investigate the effect of AMPK activation on apoptosis in differentiating myoblasts from atrophied rat soleus muscle.
  • To determine if AICAR treatment can mitigate apoptosis in these cells.

Main Methods:

  • Hindlimb suspension (HS) model in rats to induce muscle atrophy.
  • Isolation and differentiation of myoblasts from soleus muscles.
  • Treatment with AICAR to activate AMPK.
  • Evaluation of apoptosis using TUNEL assay, RT-PCR, and Western blot (WB).

Main Results:

  • Differentiating myoblasts from atrophied muscle showed decreased AMPK and ACC phosphorylation, increased apoptosis, and upregulated pro-apoptotic markers (caspase-3, -9, BAX, p53).
  • AICAR treatment normalized AMPK and ACC phosphorylation.
  • AICAR treatment prevented the increase in apoptotic nuclei and maintained pro-apoptotic marker expression at control levels.

Conclusions:

  • AMPK activity is critical in regulating apoptosis of differentiating myoblasts during muscle atrophy.
  • Maintaining AMPK activity through activation (e.g., AICAR) can suppress enhanced apoptosis in atrophied muscle-derived myoblasts.
  • This suggests a potential therapeutic target for muscle atrophy-related conditions.

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