The membrane attack complex of complement drives the progression of atherosclerosis in apolipoprotein E knockout mice

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Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
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Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

Ruth D Lewis1, Christopher L Jackson, B Paul Morgan

  • 1Department of Medical Biochemistry and Immunology, School of Medicine, Cardiff University, Cardiff, UK.

Molecular Immunology
|December 5, 2009
PubMed

Insights

Complement system

Area of Science:

  • Immunology
  • Cardiovascular Research

Background:

  • Atherosclerosis is a chronic inflammatory disease.
  • The complement system, particularly the membrane attack complex (MAC), plays a role in inflammation.
  • CD59 is a key regulator of MAC formation.

Purpose of the Study:

  • To investigate the specific roles of MAC and its regulator CD59 in atherosclerosis development.
  • To determine the impact of C6 deficiency and CD59a deficiency on atherosclerosis progression.

Main Methods:

  • Generated double knockout mouse models: C6 knockout (C6(-/-)) and CD59a knockout (Cd59a(-/-)) on an apolipoprotein E knockout (apoE(-/-)) background.
  • Fed mice a high-fat diet to induce and study atherosclerosis progression.
  • Analyzed plaque area, disease severity, MAC deposition, and smooth muscle cell proliferation.

Main Results:

  • C6 deficiency significantly reduced atherosclerotic plaque area and disease severity.
  • CD59a deficiency led to increased plaque area and severity.
  • Increased MAC deposition and smooth muscle cell proliferation were observed in CD59a-deficient mice.

Conclusions:

  • The membrane attack complex (MAC) contributes to atherosclerosis development.
  • C6 deficiency is protective against atherosclerosis.
  • CD59a deficiency exacerbates atherosclerosis, highlighting its protective role in this context.
Abstract

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