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Reactive oxygen species induce cardiomyocyte apoptosis partly through TNF-alpha

Ryuichi Aikawa1, Yuko Nitta-Komatsubara, Sumiyo Kudoh

  • 1Department of Cardiovascular Medicine, University of Tokyo Graduate School of Medicine, Tokyo, Japan.

Cytokine
|July 20, 2002
PubMed

Insights

Oxidative stress triggers cardiomyocyte apoptosis, partly via tumor necrosis factor-alpha (TNF-alpha). Blocking TNF-alpha reduced H(2)O(2)-induced cell death, suggesting its role in this process.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Biology

Background:

  • Oxidative stress is known to induce apoptosis in cardiomyocytes.
  • The precise molecular mechanisms underlying this process remain largely unelucidated.

Purpose of the Study:

  • To investigate the potential role of tumor necrosis factor-alpha (TNF-alpha) in oxidative stress-induced cardiomyocyte apoptosis.
  • To determine if TNF-alpha mediates the apoptotic effects of hydrogen peroxide (H(2)O(2)) in cardiac myocytes.

Main Methods:

  • Utilized TUNEL assay to quantify apoptosis in cardiomyocytes exposed to H(2)O(2).
  • Assessed the effect of anti-TNF-alpha antibody pretreatment on H(2)O(2)-induced apoptosis.
  • Measured TNF-alpha gene expression and protein levels in response to H(2)O(2) stimulation.

Main Results:

  • H(2)O(2) upregulated TNF-alpha gene expression and increased its concentration in the culture medium.
  • Pretreatment with anti-TNF-alpha antibody significantly reduced the number of apoptotic cardiomyocytes induced by H(2)O(2).
  • Combined stimulation with H(2)O(2) and TNF-alpha synergistically enhanced cardiomyocyte apoptosis compared to individual treatments.

Conclusions:

  • Oxidative stress, specifically H(2)O(2), induces apoptosis in cardiomyocytes partially through the involvement of TNF-alpha.
  • TNF-alpha acts as a mediator in the apoptotic pathway initiated by oxidative stress in cardiac myocytes.

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