Subphysiologic Apolipoprotein E (ApoE) plasma levels inhibit neointimal formation after arterial injury in ApoE-deficient mice

Hilke Wientgen, Fayanne E. Thorngate, Sabina Omerhodzic, Linda Rolnitzky, John T. Fallon, David L. Williams, Edward A. Fisher

Research output: Contribution to journalArticlepeer-review

26 Scopus citations


Objective - Apolipoprotein E (apoE) reduces mouse atherosclerosis progression independent of plasma cholesterol level effects. A mouse artery injury model was used to examine whether apoE exhibits beneficial lipid-independent effects on neointimal formation. Methods and Results - ApoE-deficient (apoE-/-), wild-type (WT), and transgenic apoE-/- mice (secreting apoE at different levels from adrenal glands) underwent femoral artery injury. Mice with low expression of plasma apoE (0.1% of WT) had cholesterol levels approximately half those of apoE-/- littermates (but still ≈6x >WT). Mice with higher expression (HE; 2% to 3% of WT) of plasma apoE had cholesterol levels approximately twice those of WT. Injured WT mouse (versus apoE-/-) arteries had a smaller mean intima-to-media (I/M) ratio (0.87 versus 1.96; P<0.05). HE mice tended to have lower mean I/M ratios (1.3; P>0.05 versus apoE-/- mice). Multiple regression analysis indicated that apoE levels were significantly associated with reduced I/M ratios, but plasma cholesterol levels were not, before or after adjusting for apoE. In addition, foam cell content of the neointima and media of injured arteries, a negative prognostic indicator in postangioplasty human lesions, was inversely related to plasma apoE levels. Conclusions - Similar to its effects on atherosclerosis progression, in a mouse model of restenosis, a subphysiological level of apoE was associated with beneficial effects on lesion size/composition.

Original languageEnglish
Pages (from-to)1460-1465
Number of pages6
JournalArteriosclerosis, Thrombosis, and Vascular Biology
Issue number8
StatePublished - Aug 2004


  • Apolipoprotein E
  • Arterial injury
  • Mouse
  • Neointimal formation
  • Restenosis


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