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Actin cytoskeleton as a target for 2-chloro adenosine: evidence for induction of apoptosis in C2C12 myoblastic cells

S Rufini1, G Rainaldi, M P Abbracchio

  • 1Department of Biology, University of Rome Tor Vergata, via della Ricerca Scientifica, Rome, 00133, Italy.

Insights

Adenosine analogs, like 2-chloro adenosine, trigger programmed cell death (apoptosis) in muscle cells by disrupting their internal structure. This research highlights adenosine

Area of Science:

  • Cell Biology
  • Biochemistry
  • Muscle Physiology

Background:

  • Adenosine induces apoptosis in various cell types.
  • The role of adenosine in muscle cell apoptosis remains unexplored.

Purpose of the Study:

  • Investigate the effect of 2-chloro adenosine on cultured muscle cells (C2C12).
  • Determine if adenosine analogs can induce apoptosis in myoblasts and myotubes.

Main Methods:

  • Utilized a C2C12 myogenic cell line for in vitro differentiation into myotubes.
  • Administered 2-chloro adenosine to assess its impact on cell viability and morphology.
  • Examined actin microfilament integrity and its correlation with apoptotic events.

Main Results:

  • 2-chloro adenosine induced apoptosis in both C2C12 myoblasts and differentiated myotubes.
  • Apoptosis was preceded by significant alterations in actin microfilaments.
  • Observed a time-dependent relationship between cytoskeletal derangement and apoptosis induction.

Conclusions:

  • Adenosine acts as an endogenous regulator of apoptosis in muscle cells.
  • Cytoskeletal integrity is crucial for muscle cell survival.
  • The C2C12 cell model is valuable for studying muscle cell pathologies involving apoptosis.

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