Human apolipoprotein A-II is a pro-atherogenic molecule when it is expressed in transgenic mice at a level similar to that in humans: Evidence of a potentially relevant species-specific interaction with diet

Joan Carles Escolá-Gil, Àfrica Marzal-Casacuberta, Josep Julve-Gil, Brian Y. Ishida, Jordi Ordóñez-Llanos, Lawrence Chan, Francesc González-Sastre, Francisco Blanco-Vaca

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65 Citations (Scopus)

Abstract

We report on the effect of human apolipoprotein (apo) A-II transgene expression on atherosclerosis susceptibility in two transgenic lines (25.3 and 11.1) whose plasma human apoA-II concentrations (~23 and 96 mg/dl, respectively) span the normal range in humans. After 9 months of an atherogenic diet, 25.3 and 11.1 transgenic mice developed aortic atherosclerotic lesions that were ~1.7- and 7-fold, respectively, more extensive than those of non-transgenic control mice. However, there was no difference in the area of atherosclerosis of transgenic and control mice when fed a regular chow diet. This contrasts with the findings in murine apoA-II transgenic mice and provides evidence of a species-specific characteristic that could be of relevance with respect to the high fat intake diets common in most industrialized countries. A possible mechanism of the pro- atherogenic action of human apoA-II could be the inhibition of reverse cholesterol transport and, in support of this, we observed an impairment of apoA-I-HDL particle interconversion in the plasma of 11.1 transgenic mice caused, at least in part, by a marked decrease in the endogenous lecithin:cholesterol acyltransferase activity.
Original languageEnglish
Pages (from-to)457-462
JournalJournal of Lipid Research
Volume39
Issue number2
Publication statusPublished - 1 Feb 1998

Keywords

  • Apolipoprotein A- I
  • Atherosclerosis
  • High density lipoproteins
  • Lecithin:cholesterol acyltransferase

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