Inhibition of early atherogenesis in transgenic mice by human apolipoprotein AI

Nature. 1991 Sep 19;353(6341):265-7. doi: 10.1038/353265a0.


Epidemiological surveys have identified a strong inverse relationship between the amount in the plasma of high density lipoproteins (HDL), apolipoprotein AI (ApoA-I), the major protein component of HDL, and the risk for atherosclerosis in humans. It is not known if this relationship arises from a direct antiatherogenic effect of these plasma components or if it is the result of other factors also associated with increases in ApoA-I and HDL levels. Because some strains of mice are susceptible to diet-induced formation of preatherosclerotic fatty streak lesions, and because of available techniques for the genetic manipulation of this organism, the murine system offers a unique setting in which to investigate the process of early atherogenesis. To test the hypothesis that induction of a high plasma concentration of ApoA-I and HDL would inhibit this process, we studied the effects of atherogenic diets on transgenic mice expressing high amounts of human ApoA-I. We report that transgenic mice with high plasma ApoA-I and HDL levels were significantly protected from the development of fatty streak lesions.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Aorta / pathology*
  • Apolipoprotein A-I
  • Apolipoproteins A / blood
  • Apolipoproteins A / genetics*
  • Arteriosclerosis / genetics*
  • Arteriosclerosis / pathology
  • Arteriosclerosis / physiopathology
  • Butter*
  • Cholesterol, Dietary*
  • Diet, Atherogenic*
  • Genetic Predisposition to Disease
  • Humans
  • Lipoproteins, HDL / genetics*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Muscle, Smooth, Vascular / pathology


  • Apolipoprotein A-I
  • Apolipoproteins A
  • Cholesterol, Dietary
  • Lipoproteins, HDL
  • Butter