Plasmalogen modulation attenuates atherosclerosis in ApoE- and ApoE/GPx1-deficient mice

Atherosclerosis. 2015 Dec;243(2):598-608. doi: 10.1016/j.atherosclerosis.2015.10.096. Epub 2015 Oct 26.

Abstract

Background and aim: We previously reported a negative association of circulating plasmalogens (phospholipids with proposed atheroprotective properties) with coronary artery disease. Plasmalogen modulation was previously demonstrated in animals but its effect on atherosclerosis was unknown. We assessed the effect of plasmalogen enrichment on atherosclerosis of murine models with differing levels of oxidative stress.

Methods and results: Six-week old ApoE- and ApoE/glutathione peroxidase-1 (GPx1)-deficient mice were fed a high-fat diet with/without 2% batyl alcohol (precursor to plasmalogen synthesis) for 12 weeks. Mass spectrometry analysis of lipids showed that batyl alcohol supplementation to ApoE- and ApoE/GPx1-deficient mice increased the total plasmalogen levels in both plasma and heart. Oxidation of plasmalogen in the treated mice was evident from increased level of plasmalogen oxidative by-product, sn-2 lysophospholipids. Atherosclerotic plaque in the aorta was reduced by 70% (P = 5.69E-07) and 69% (P = 2.00E-04) in treated ApoE- and ApoE/GPx1-deficient mice, respectively. A 40% reduction in plaque (P = 7.74E-03) was also seen in the aortic sinus of only the treated ApoE/GPx1-deficient mice. Only the treated ApoE/GPx1-deficient mice showed a decrease in VCAM-1 staining (-28%, P = 2.43E-02) in the aortic sinus and nitrotyrosine staining (-78%, P = 5.11E-06) in the aorta.

Conclusion: Plasmalogen enrichment via batyl alcohol supplementation attenuated atherosclerosis in ApoE- and ApoE/GPx1-deficient mice, with a greater effect in the latter group. Plasmalogen enrichment may represent a viable therapeutic strategy to prevent atherosclerosis and reduce cardiovascular disease risk, particularly under conditions of elevated oxidative stress and inflammation.

Keywords: Alkenylphospholipid; Alkylphospholipid; Anti-oxidant; Atherosclerosis; Batyl alcohol; Lipidomics; Plasmalogen.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aorta / drug effects
  • Aorta / enzymology
  • Aorta / pathology
  • Aortic Diseases / blood
  • Aortic Diseases / enzymology
  • Aortic Diseases / genetics
  • Aortic Diseases / pathology
  • Aortic Diseases / prevention & control*
  • Apolipoproteins E / deficiency*
  • Apolipoproteins E / genetics
  • Atherosclerosis / blood
  • Atherosclerosis / enzymology
  • Atherosclerosis / genetics
  • Atherosclerosis / pathology
  • Atherosclerosis / prevention & control*
  • Cholesterol / blood
  • Diet, High-Fat
  • Disease Models, Animal
  • Glutathione Peroxidase / deficiency*
  • Glutathione Peroxidase / genetics
  • Glutathione Peroxidase GPX1
  • Glyceryl Ethers / metabolism
  • Glyceryl Ethers / pharmacology*
  • Inflammation Mediators / metabolism
  • Lysophospholipids / blood
  • Male
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Myocardium / enzymology
  • Oxidation-Reduction
  • Oxidative Stress
  • Plaque, Atherosclerotic
  • Plasmalogens / blood*
  • Tyrosine / analogs & derivatives
  • Tyrosine / metabolism
  • Up-Regulation
  • Vascular Cell Adhesion Molecule-1 / metabolism

Substances

  • Apolipoproteins E
  • Glyceryl Ethers
  • Inflammation Mediators
  • Lysophospholipids
  • Plasmalogens
  • Vascular Cell Adhesion Molecule-1
  • 3-nitrotyrosine
  • batyl alcohol
  • Tyrosine
  • Cholesterol
  • Glutathione Peroxidase
  • Glutathione Peroxidase GPX1
  • Gpx1 protein, mouse