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Independent protective roles for macrophage Abcg1 and Apoe in the atherosclerotic lesion development

Bart Lammers1, Ruud Out, Reeni B Hildebrand

  • 1Gorlaeus Leiden/Amsterdam Center for Drug Research, Leiden University, The Netherlands. b.lammers@lacdr.leidenuniv.nl

Atherosclerosis
|February 17, 2009
PubMed

Insights

Combined deletion of ATP-binding cassette transporter G1 (Abcg1) and apolipoprotein E (Apoe) significantly increases atherosclerosis. These proteins have an additive, independent effect in preventing atherosclerosis development.

Area of Science:

  • Cardiovascular Biology
  • Lipid Metabolism
  • Atherosclerosis Research

Background:

  • ATP-binding cassette transporter G1 (Abcg1) and apolipoprotein E (Apoe) are key in macrophage cholesterol efflux.
  • Their roles in atherosclerosis development and potential interaction are not fully understood.

Purpose of the Study:

  • To investigate the combined effect of Abcg1 and Apoe on atherosclerotic lesion formation.
  • To determine if Abcg1 and Apoe have additive or interactive roles in preventing atherosclerosis.

Main Methods:

  • Bone marrow from Abcg1/Apoe double knockout (dKO), single knockout, and wild-type mice were transplanted into LDL receptor knockout mice.
  • Mice were fed a high-fat/high-cholesterol diet to induce atherosclerosis.
  • In vitro macrophage cholesterol efflux assays were performed.

Main Results:

  • Combined deletion of Abcg1 and Apoe significantly increased atherosclerotic lesion area compared to single knockouts and wild-type controls.
  • Serum lipid levels showed no significant differences between groups.
  • In vitro studies confirmed that combined Abcg1 and Apoe deletion markedly reduced cholesterol efflux to HDL.

Conclusions:

  • Macrophage Abcg1 and Apoe exhibit an additive and independent effect in preventing atherosclerosis.
  • Combined deficiency of Abcg1 and Apoe dramatically exacerbates atherosclerosis development.
Abstract

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