Effects of adenovirus-mediated human apo A-I gene transfer on neointima formation after endothelial denudation in apo E-deficient mice

Circulation
Bart De GeestP Holvoet

Abstract

Inactivation of apolipoprotein (apo) E genes in mice markedly increases beta-VLDL levels and accelerates progression of complex atherosclerotic lesions. The present study investigated (1) the effect of apo E deficiency (apo E-/-) on neointima formation after endothelial denudation; and (2) the effect of increased HDL, induced by adenovirus-mediated transfer of a human apo A-I gene, on neointima formation. Guidewire-induced abrasion of the endothelium of the common carotid artery did not produce neointima formation within 18 days after injury in C57BL/6J mice (n=12) but was associated with an intima/media ratio of 0.82+/-0.25 in age-matched C57BL/6J apo E-/- mice (n=12). Neointima consisted primarily of smooth muscle alpha-actin positive cells. Injection in C57BL/6J apo E-/- mice of 2x10(9) (n=5) or 4x10(9) (n=7) plaque forming units (p.f.u.) of a recombinant human apo A-I adenovirus 3 days before injury resulted in an increase of HDL cholesterol from 36+/-5 to 75+/-3 mg/dL (P<.05) and to 96+/-13 mg/dL (P<.05), respectively, and of the HDL cholesterol/non-HDL cholesterol ratio from 0.063+/-0.003 to 0.15+/-0.01 (P<.05) and to 0.16+/-0.015 (P<.05), respectively. Intima/media ratio decreased to 0.28+/-0.06 (P=NS versus C57BL/6J apo...Continue Reading

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