Remnant lipoproteins induce proatherothrombogenic molecules in endothelial cells through a redox-sensitive mechanism

Circulation. 2000 Aug 8;102(6):670-6. doi: 10.1161/01.cir.102.6.670.

Abstract

Background: Triglyceride-rich lipoproteins (TGLs) are atherogenic. However, their cellular mechanisms remain largely unexplained. This study examined the effects of isolated remnant-like lipoprotein particles (RLPs) on the expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and tissue factor (TF), proatherothrombogenic molecules, in cultured human endothelial cells.

Methods and results: RLPs were isolated from plasma of hypertriglyceridemic patients by use of the immunoaffinity gel mixture of anti-apoA-1 and anti-apoB-100 monoclonal antibodies. The incubation of cells with RLPs significantly upregulated mRNA and protein expression of these molecules. Total TGLs (d<1.006) and LDL had fewer or minimal effects on expression of these molecules compared with RLPs. RLPs increased intracellular oxidant levels, as assessed with an oxidant-sensitive probe. Combined incubation with alpha-tocopherol or N-acetylcysteine, both antioxidants, suppressed RLP-induced increase in expression of these molecules. In patients with higher plasma levels of RLPs, plasma levels of soluble forms of ICAM-1 and VCAM-1 were significantly higher than in patients with lower RLP levels. Treatment with alpha-tocopherol for 1 month decreased levels of the soluble adhesion molecules concomitantly with an increase in resistance of RLPs to oxidative modification in patients with high RLP levels.

Conclusions: RLPs upregulated endothelial expression of ICAM-1, VCAM-1, and TF, proatherothrombogenic molecules, partly through a redox-sensitive mechanism. RLPs may have an important role in atherothrombotic complications in hypertriglyceridemic patients.

Publication types

  • Clinical Trial
  • Randomized Controlled Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Arteriosclerosis / drug therapy
  • Arteriosclerosis / etiology*
  • Cells, Cultured
  • Culture Media / metabolism
  • DNA / metabolism
  • Endothelium, Vascular / cytology
  • Endothelium, Vascular / metabolism*
  • Humans
  • Hypertriglyceridemia / blood
  • Intercellular Adhesion Molecule-1 / blood
  • Intercellular Adhesion Molecule-1 / genetics
  • Intercellular Adhesion Molecule-1 / metabolism
  • Lipid Peroxides / metabolism
  • Lipoproteins / blood
  • Lipoproteins / physiology*
  • NF-kappa B / metabolism
  • Oxidation-Reduction
  • Peptide Fragments / blood
  • Peptide Fragments / physiology
  • RNA, Messenger / metabolism
  • Solubility
  • Thromboplastin / genetics
  • Thromboplastin / metabolism
  • Vascular Cell Adhesion Molecule-1 / blood
  • Vascular Cell Adhesion Molecule-1 / genetics
  • Vascular Cell Adhesion Molecule-1 / metabolism
  • Vitamin E / therapeutic use

Substances

  • Culture Media
  • Lipid Peroxides
  • Lipoproteins
  • NF-kappa B
  • Peptide Fragments
  • RNA, Messenger
  • Vascular Cell Adhesion Molecule-1
  • Intercellular Adhesion Molecule-1
  • Vitamin E
  • DNA
  • Thromboplastin