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Ceramide path in human lung cell death.

C Chan1, T Goldkorn

  • 1Signal Transduction, Department of Medicine, University of California Davis School of Medicine, Davis, CA 95616, USA.

American Journal of Respiratory Cell and Molecular Biology
|April 4, 2000
PubMed
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Hydrogen peroxide (H2O2) triggers apoptosis in human airway epithelial cells by increasing ceramide. Protein kinase C (PKC) inhibits this H2O2-induced ceramide production and cell death, suggesting a key role in lung inflammation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Pulmonary Medicine

Background:

  • Lung epithelium modulates inflammatory responses to injury.
  • Airway epithelial cells are targets of reactive oxygen species like hydrogen peroxide (H2O2).
  • Mechanisms of H2O2 effects on epithelial cells are not fully understood.

Purpose of the Study:

  • To investigate the role of sphingomyelin (SM) hydrolysis and ceramide generation in H2O2-induced apoptosis of human airway epithelial (HAE) cells.
  • To determine the involvement of protein kinase C (PKC) in modulating H2O2-induced apoptosis.

Main Methods:

  • Exposure of HAE cells to varying concentrations of H2O2.
  • Measurement of neutral sphingomyelinase activity, SM hydrolysis, and ceramide generation.
  • Assessment of apoptosis induction and modulation by PKC activation and C6-ceramide addition.

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Main Results:

  • H2O2 exposure (50-100 microM) rapidly activated neutral sphingomyelinase, leading to SM hydrolysis, ceramide generation, and apoptosis in HAE cells.
  • Activation of PKC by 12-O-tetradecanoylphorbol-13-acetate inhibited H2O2-induced ceramide production and apoptosis.
  • Addition of cell-permeant C6-ceramide restored the apoptotic response, confirming ceramide's role.

Conclusions:

  • Ceramide, generated via SM hydrolysis, is a key mediator of H2O2-induced apoptosis in airway epithelial cells.
  • PKC activation counteracts ceramide-mediated apoptosis in these cells.
  • Ceramide-mediated apoptosis and its inhibition by PKC represent a significant mechanism in modulating lung inflammatory processes.