Reverse D4F, an apolipoprotein-AI mimetic peptide, inhibits atherosclerosis in ApoE-null mice

J Cardiovasc Pharmacol Ther. 2012 Sep;17(3):334-43. doi: 10.1177/1074248411434598. Epub 2012 Feb 3.

Abstract

Objective: Synthetic class A amphipathic helical peptide analogs of apolipoprotein-AI (apoAI; with varied phenylalanine residues) are emerging therapeutic approaches under investigation for atherosclerosis. Utilizing retroinverso sequencing, we designed reverse-D4F (Rev-D4F) peptide with 18 d-amino acids containing 4 phenylalanine residues and reverse order that allows the side chain residues to be of exact alignment and superimposable to those of the parent l-amino acid peptide. This study examined the effect of Rev-D4F on atherosclerosis in apolipoprotein E (apoE)-null mice and the underlying mechanisms.

Materials/methods: ApoE-null mice were fed a chow diet and administered water (control), Rev-D4F, or L4F mimetic peptides (0.4 mg/mL, equivalent to 1.6 mg/d) orally in drinking water for 6 weeks. Aortic root atherosclerotic lesion area, lesion macrophage content, and the ability of plasma high-density lipoprotein (HDL) to influence monocyte chemotaxis were measured.

Results: Rev-D4F significantly decreased aortic sinus atherosclerotic lesion area and lesion macrophage content without affecting plasma total and HDL-cholesterol levels in apoE-null mice. The HDL from Rev-D4F-treated mice showed enhanced anti-inflammatory monocyte chemotactic activity, while low-density lipoprotein (LDL) exhibited reduced proinflammatory activity. In in vitro studies, Rev-D4F inhibited LDL oxidation, endothelial cell vascular cell adhesion molecule 1 (VCAM-1), and monocyte chemotactic factor 1 (MCP-1) expression, and monocyte adhesion to aortic endothelial cells.

Conclusions: The Rev-D4F inhibits atherosclerosis by inhibiting endothelial inflammatory/oxidative events and improving HDL function. The data suggest that Rev-D4F may be an effective apoAI mimetic peptide for further development in preventing atherosclerosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aorta / cytology
  • Apolipoprotein A-I / pharmacology*
  • Apolipoproteins E / genetics
  • Apolipoproteins E / metabolism*
  • Atherosclerosis / prevention & control*
  • Body Weight / drug effects
  • Chemokine CCL2 / genetics
  • Chemokine CCL2 / metabolism
  • Coculture Techniques
  • Endothelial Cells
  • Female
  • Humans
  • Lipids / blood
  • Macrophages / drug effects
  • Mice
  • Mice, Knockout
  • Peptides / pharmacology*

Substances

  • Apolipoprotein A-I
  • Apolipoproteins E
  • Ccl2 protein, mouse
  • Chemokine CCL2
  • D-4F peptide
  • L-4F peptide
  • Lipids
  • Peptides
  • reverse-D-4F peptide