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The apoptotic regulatory protein ARC (apoptosis repressor with caspase recruitment domain) prevents oxidant

M Neuss1, R Monticone, M S Lundberg

  • 1Department of Medicine/Cardiology, German Heart Institute, 13353 Berlin, Germany.

The Journal of Biological Chemistry
|July 5, 2001
PubMed

Insights

The apoptotic regulatory protein ARC protects cells from hydrogen peroxide-induced death. ARC prevents mitochondrial dysfunction and cell death, demonstrating a role in blocking necrosis-like cell death by preserving mitochondrial function.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • The apoptotic regulatory protein ARC is primarily expressed in myogenic cells.
  • ARC contains a caspase recruitment domain (CARD) and inhibits initiator caspases.
  • ARC also inhibits caspase-independent apoptotic events, such as hypoxia-induced cytochrome c release.

Purpose of the Study:

  • To investigate the role of ARC in hydrogen peroxide (H(2)O(2))-induced cell death in the H9c2 myogenic cell line.
  • To determine if ARC can prevent necrosis-like cell death.
  • To elucidate the mechanism by which ARC exerts its protective effects.

Main Methods:

  • Exposure of H9c2 cells to H(2)O(2) to induce cell death.
  • Analysis of ARC expression levels during H(2)O(2)-induced cell death.
  • Assessment of mitochondrial membrane potential (Delta psi(m)) and plasma membrane integrity.
  • Ectopic expression of ARC in H9c2 and human cell lines.
  • Evaluation of stress kinase response.

Main Results:

  • H(2)O(2)-induced cell death in H9c2 cells was caspase-independent and characterized by reduced ARC expression, mitochondrial dysfunction, and loss of plasma membrane integrity.
  • Ectopic expression of ARC prevented H(2)O(2)-induced mitochondrial dysfunction and cell death.
  • ARC's protective effects were observed downstream of early signaling events and did not involve quenching of H(2)O(2).
  • ARC also protected other human cell lines from H(2)O(2)-induced damage.

Conclusions:

  • ARC prevents necrosis-like cell death induced by H(2)O(2).
  • ARC preserves mitochondrial function, thereby blocking cell death.
  • ARC's protective role extends beyond apoptosis to include necrosis-like cell death pathways.

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