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Decrease in the expression of muscle-specific miRNAs, miR-133a and miR-1, in myoblasts with replicative senescence.

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Cellular senescence impairs muscle regeneration by reducing microRNAs (miRNAs) miR-1 and miR-133a in myoblasts. Restoring these muscle-specific miRNAs can improve myoblast differentiation and fusion, crucial for muscle repair.

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Area of Science:

  • Muscle biology and regeneration
  • Cellular senescence
  • MicroRNA biology

Background:

  • Aging and muscle injury trigger myogenic regeneration, a process involving myoblasts.
  • Myoblast function declines with age, impairing regeneration.
  • MicroRNAs (miRNAs), including muscle-specific miR-1 and miR-133a, regulate myoblast proliferation and differentiation.

Purpose of the Study:

  • To investigate the impact of cellular senescence on miR-1 and miR-133a expression in myoblasts.
  • To determine if altered miRNA levels contribute to impaired myogenic differentiation in senescent myoblasts.

Main Methods:

  • C2C12 murine skeletal myoblasts were induced into replicative senescence.
  • miR-1 and miR-133a expression levels were analyzed in senescent and non-senescent myoblasts.
  • Myogenic differentiation, cell fusion, and the effect of a glutaminase 1 inhibitor (BPTES) were assessed.
  • Primary myoblasts from young and aged mice were compared for miRNA levels.

Main Results:

  • miR-1 and miR-133a expression, typically induced during differentiation, was suppressed in senescent myoblasts.
  • Senescent myoblasts showed impaired myogenic differentiation and cell fusion.
  • Transfection of miR-1 or miR-133a ameliorated cell fusion defects in senescent myoblasts.
  • BPTES treatment reduced senescent cells, increased myotube formation, and elevated miR-133a levels.
  • Primary myoblasts from aged mice had lower miR-1 and miR-133a levels compared to younger mice.

Conclusions:

  • Replicative senescence suppresses muscle-specific miRNA expression (miR-1, miR-133a) in myoblasts.
  • This suppression contributes to the age-related decline in myogenic regeneration.
  • Targeting senescence or restoring these miRNAs may offer therapeutic strategies for muscle repair.