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Fragmentation of DNA in P388D1 macrophages exposed to oxidised low-density lipoprotein

V C Reid1, S J Hardwick, M J Mitchinson

  • 1Department of Pathology, University of Cambridge, UK.

FEBS Letters
|October 18, 1993
PubMed

Insights

Copper-oxidized LDL triggers DNA damage in macrophages, a process inhibited by zinc sulfate. This suggests apoptosis is a key mechanism in macrophage foam cell death within atherosclerotic lesions.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pathology

Background:

  • Macrophage foam cell accumulation is central to atherosclerosis.
  • The precise mechanism of foam cell death in arterial lesions remains unclear.

Purpose of the Study:

  • To investigate the mechanism of cell death induced by copper-oxidized low-density lipoprotein (oxLDL) in macrophages.
  • To determine if apoptosis is involved in macrophage foam cell death.

Main Methods:

  • A macrophage-like murine cell line was exposed to copper-oxidized low-density lipoprotein (oxLDL).
  • DNA fragmentation was assessed.
  • The effect of zinc sulfate, a Ca2+/Mg2+ endonuclease inhibitor, was evaluated.
  • Membrane impermeability was monitored.

Main Results:

  • Exposure to copper-oxLDL induced significant DNA fragmentation in macrophages.
  • Zinc sulfate treatment inhibited this DNA fragmentation.
  • DNA fragmentation was observed before the loss of membrane integrity.
  • These findings indicate an apoptotic pathway.

Conclusions:

  • Copper-oxidized low-density lipoprotein induces apoptosis in macrophages.
  • Apoptosis may be a significant mechanism contributing to macrophage foam cell death in atherosclerotic plaques.
  • Targeting this apoptotic pathway could offer therapeutic strategies for atherosclerosis.

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