The apolipoprotein A-I mimetic peptide, ETC-642, reduces chronic vascular inflammation in the rabbit

Lipids Health Dis. 2011 Nov 30:10:224. doi: 10.1186/1476-511X-10-224.

Abstract

Background: High-density lipoproteins (HDL) and their main apolipoprotein, apoA-I, exhibit anti-inflammatory properties. The development of peptides that mimic HDL apolipoproteins offers a promising strategy to reduce inflammatory disease. This study aimed to compare the anti-inflammatory effects of ETC-642, an apoA-I mimetic peptide, with that of discoidal reconstituted HDL (rHDL), consisting of full-length apoA-I complexed with phosphatidylcholine, in rabbits with chronic vascular inflammation.

Results: New Zealand White rabbits (n = 10/group) were placed on chow supplemented with 0.2% (w/w) cholesterol for 6-weeks. The animals received two infusions of saline, rHDL (8 mg/kg apoA-I) or ETC-642 (30 mg/kg peptide) on the third and fifth days of the final week. The infusions of rHDL and ETC-642 were able to significantly reduce cholesterol-induced expression of intracellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in the thoracic aorta (p < 0.05). When isolated rabbit HDL was pre-incubated with human coronary artery endothelial cells (HCAECs), prior to stimulation with TNF-α, it was found that HDL from ETC-642 treated rabbits were more effective at inhibiting the TNF-α-induced increase in ICAM-1, VCAM-1 and p65 than HDL isolated from saline treated rabbits (p < 0.05). There were, however, no changes in HDL lipid composition between treatment groups.

Conclusions: Infusion of ETC-642 causes anti-inflammatory effects that are comparable to rHDL in an animal model of chronic vascular inflammation and highlights that apoA-I mimetic peptides present a viable strategy for the treatment of inflammatory disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 1,2-Dipalmitoylphosphatidylcholine / pharmacology*
  • 1,2-Dipalmitoylphosphatidylcholine / therapeutic use
  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Anti-Inflammatory Agents / therapeutic use
  • Aorta, Thoracic / drug effects
  • Aorta, Thoracic / pathology
  • Apolipoprotein A-I / pharmacology*
  • Apolipoprotein A-I / therapeutic use
  • Cells, Cultured
  • Cholesterol / blood
  • Chronic Disease
  • Endothelial Cells / drug effects
  • Endothelial Cells / metabolism
  • Gene Expression / drug effects
  • Humans
  • Inflammation / chemically induced
  • Inflammation / drug therapy*
  • Intercellular Adhesion Molecule-1 / genetics
  • Intercellular Adhesion Molecule-1 / metabolism
  • Lipoproteins, HDL / pharmacology*
  • Lipoproteins, HDL / therapeutic use
  • Male
  • Peptides / pharmacology*
  • Peptides / therapeutic use
  • Rabbits
  • Random Allocation
  • Sphingomyelins / pharmacology*
  • Sphingomyelins / therapeutic use
  • Transcription Factor RelA / genetics
  • Transcription Factor RelA / metabolism
  • Vascular Cell Adhesion Molecule-1 / genetics
  • Vascular Cell Adhesion Molecule-1 / metabolism

Substances

  • Anti-Inflammatory Agents
  • Apolipoprotein A-I
  • ETC 642
  • Lipoproteins, HDL
  • Peptides
  • Sphingomyelins
  • Transcription Factor RelA
  • Vascular Cell Adhesion Molecule-1
  • Intercellular Adhesion Molecule-1
  • 1,2-Dipalmitoylphosphatidylcholine
  • Cholesterol