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Angiopoietin-1 protects H9c2 cells from H2O2-induced apoptosis through AKT signaling

Zuoyan Wang1, Ming Cui, Lijie Sun

  • 1Department of Cardiology, Peking University Third Hospital, Beijing 100083, China.

Biochemical and Biophysical Research Communications
|June 15, 2007
PubMed

Insights

Angiopoietin-1 (Ang1) protects heart cells from oxidative stress-induced cell death. This protective effect involves regulating the AKT pathway, offering potential therapeutic insights for heart failure.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Biology

Background:

  • Cardiomyocyte apoptosis contributes to ventricular remodeling and heart failure.
  • Reactive oxygen species (ROS) are implicated in pathological cardiac processes via apoptosis.
  • Angiopoietin-1 (Ang1) is a potential therapeutic agent for cardiovascular diseases.

Purpose of the Study:

  • To investigate the direct cytoprotective effects of Angiopoietin-1 (Ang1) on cardiomyocytes against oxidative stress.
  • To elucidate the molecular mechanisms underlying Ang1's protective action in cardiomyocytes.

Main Methods:

  • Cultured H9c2 cells (cardiomyocytes) were exposed to hydrogen peroxide (H(2)O(2)) to induce oxidative stress.
  • Apoptosis was assessed using flow cytometry, TUNEL assay, and DNA laddering.
  • The role of AKT signaling was examined through gene expression and inhibition studies.

Main Results:

  • H(2)O(2) treatment induced time-dependent apoptosis in H9c2 cells.
  • Overexpression of Ang1 via adenovirus inhibited H(2)O(2)-induced apoptosis.
  • Ang1 treatment led to sustained AKT phosphorylation, which was reversed by AKT inhibition.

Conclusions:

  • Angiopoietin-1 (Ang1) demonstrates direct cytoprotective effects on cardiomyocytes against oxidative stress.
  • The protective mechanism of Ang1 involves the regulation of AKT pathway activity.
  • These findings suggest Ang1 as a potential therapeutic target for preventing heart failure progression.

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