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Nitric oxide induces apoptosis in mouse C2C12 myoblast cells

Myoung-Hwa Lee1, Mi-Hyeon Jang, Eun-Kyung Kim

  • 1Department of Physiology, College of Medicine, Kyung Hee University, Seoul, Korea.

Journal of Pharmacological Sciences
|March 23, 2005
PubMed

Insights

Nitric oxide (NO) triggers apoptosis in myoblast cells. This cell death involves the p53, bax, and caspase pathways, confirmed by various assays in mouse C2C12 cells.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Nitric oxide (NO) plays diverse roles in cellular signaling.
  • Apoptosis, or programmed cell death, is crucial for tissue homeostasis.
  • Myoblast cells are essential for muscle development and repair.

Purpose of the Study:

  • To determine if nitric oxide (NO) induces apoptosis in myoblast cells.
  • To elucidate the molecular mechanisms underlying NO-induced apoptosis in myoblasts.

Main Methods:

  • Utilized sodium nitroprusside (SNP) as an NO donor.
  • Employed MTT assay, flow cytometry, DAPI staining, TUNEL assay, and DNA fragmentation analysis.
  • Conducted RT-PCR, Western blot, and caspase-3 enzyme assays to assess molecular changes.

Main Results:

  • SNP treatment induced significant apoptotic features in C2C12 myoblast cells.
  • Observed increased expression of p53 and bax proteins following SNP treatment.
  • Demonstrated enhanced caspase-3 enzyme activity, indicating pathway activation.

Conclusions:

  • Nitric oxide (NO) can induce apoptotic cell death in myoblast cells.
  • The process is mediated through the activation of p53, bax, and caspase-dependent pathways.
  • Findings highlight NO's role in regulating myoblast cell fate.

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