Antiatherogenic effects of newly developed apolipoprotein A-I mimetic peptide/phospholipid complexes against aortic plaque burden in Watanabe-heritable hyperlipidemic rabbits

Atherosclerosis. 2011 Oct;218(2):300-7. doi: 10.1016/j.atherosclerosis.2011.05.029. Epub 2011 Jun 1.

Abstract

This study analyzed the antiatherogenic effects of newly developed apolipoprotein A-I (ApoA-I) mimetic peptide/phospholipid complexes (ETC-642) against the aortic plaque burden in vivo. We used human macrophage cells to analyze cholesterol efflux by ETC-642. Watanabe-heritable hyperlipidemic (WHHL) rabbits were divided into 3 groups: low- (15mg/kg) and high-dose ETC-642 (50mg/kg), and placebo. The test material was injected twice/week for 12 weeks. The aortic plaque burden was assessed by intravascular ultrasound (IVUS) at 0 and 12 weeks. Plasma lipid profiles were analyzed by capillary isotachophoresis every 4 weeks. ETC-642 had an effect on cholesterol efflux comparable to that of conventional rHDL. In WHHL rabbits, high-dose ETC-642 inhibited the progression of aortic atherosclerosis compared to placebo. There was no change in the percentage of plaque volume (%PV) in the high-dose group between before (30.9%) and after infusion (28.6%), whereas there was a significant increase in the control group from 27.8% to 37.9%. ETC-642 significantly reduced charge-modified low-density lipoprotein (LDL) by converting more negative-charged modified LDL to less negative-charged LDL, and reduced small dense (sd) LDL by converting it into large, buoyant (lb) LDL. Changes in the %PV were positively correlated with changes in negative-charged modified LDL (r=0.61, p<0.01) and sdLDL (r=0.59, p<0.01), and negatively correlated with changes in less negative-charged LDL (r=-0.43, p<0.01) and lbLDL (r=-0.57, p<0.01). In conclusion, the ETC-642-induced remodeling of sdLDL to large and lbLDL and the enhancement of cholesterol efflux may prevent progression of the aortic plaque burden. HDL-based therapy may be useful for preventing the progression of plaque volume.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aorta / pathology
  • Apolipoprotein A-I / metabolism*
  • Atherosclerosis / pathology*
  • Cholesterol / chemistry
  • Cholesterol / metabolism
  • Disease Models, Animal
  • Disease Progression
  • Humans
  • Hyperlipidemias / drug therapy*
  • Hyperlipidemias / genetics*
  • Isotachophoresis / methods
  • Lipoproteins, LDL / chemistry
  • Peptides / chemistry*
  • Placebos
  • Rabbits
  • Ultrasonography, Interventional / methods

Substances

  • Apolipoprotein A-I
  • Lipoproteins, LDL
  • Peptides
  • Placebos
  • Cholesterol