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Complement activation by oxidatively modified low-density lipoproteins.

E Wieland1, B Dorweiler, U Bonitz

  • 1Georg-August-Universität, Göttingen, Germany. ewieland@med.uni-goettingen.de

European Journal of Clinical Investigation
|December 3, 1999
PubMed
Summary
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Oxidized low-density lipoproteins (LDLs) show minimal complement activation, suggesting they are not the primary cause of complement activation in atherosclerosis. Lesion complement activators are likely unrelated to oxidized LDLs.

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Biochemistry

Background:

  • Oxidatively modified low-density lipoproteins (LDLs) are implicated in atherosclerosis pathogenesis.
  • Complement activation is increasingly recognized as a factor in atherogenesis.
  • Lesion complement activators (LCAs) are lipids found in atherosclerotic lesions that activate complement.

Purpose of the Study:

  • To investigate whether oxidized LDLs activate complement.
  • To compare the complement-activating capacity of oxidized LDLs with lesion complement activators.

Main Methods:

  • Assessed complement activation by measuring SC5b-9 formation in normal human serum.
  • Quantified C3 conversion using two-dimensional immunoelectrophoresis.
  • Tested minimally and heavily oxidized LDL preparations, native LDL, and LCA.

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Main Results:

  • Both minimally and heavily oxidized LDLs generated small but significant amounts of SC5b-9 compared to native LDL.
  • Lesion complement activator generated substantially larger amounts of SC5b-9.
  • Oxidized LDL preparations caused only minor C3 conversion.

Conclusions:

  • Oxidation does not confer significant complement-activating properties on LDL.
  • The lesion complement activator is likely not directly related to oxidized LDL.
  • Oxidized LDL plays a minor role in complement activation within atherosclerotic lesions.