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A more recent version of this article appeared on October 1, 2005

Papers In Press, published online ahead of print August 1, 2005
J. Lipid Res., doi:10.1194/jlr.M500177-JLR200
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Submitted on May 5, 2005
Revised on July 8, 2005
Accepted on July 26, 2005

Apolipoprotein E inhibition of vascular cell proliferation and neointimal formation in vivo requires inducible nitric oxide synthase

Zachary W.Q. Moore and David Y. Hui

Department of Pathology, Genome Research Institute (ML 0507), Cincinnati, OH 45237-0507

Corresponding Author: huidy{at}email.uc.edu

Previous studies have shown apolipoprotein E (apoE) recruitment to the medial layers of carotid arteries after vascular injury in vivo and apoE activation of inducible nitric oxide synthase (iNOS) expression in smooth muscle cells in vitro. This investigation explored the relationship between medial apoE recruitment, iNOS activation, and their protection against neointimal hyperplasia. ApoE was shown to be present in both the neointimal-resistant C57BL/6 mice and the neointimal-susceptible FVB/N mice 24 hr after carotid denudation, but iNOS expression was observed only in the neointimal-resistant C57BL/6 mice. However, iNOS was not observed in C57BL/6 mice without a functional apoE gene. In contrast, transgenic over-expression of apoE in FVB/N mice also activated iNOS expression in the injured vessels resulting in protection against neointimal hyperplasia. ApoE and iNOS were colocalized in the medial layer of neointimal-resistant mouse strains. Endothelial denudation of carotid arteries in the iNOS-deficient NOS2-/- mice did not increase neointimal hyperplasia but a significant increase in medial thickness and area was observed. The iNOS-specific inhibitor also abrogated the apoE protective effects on vascular response to injury in the apoE over-expressing transgenic FVB/N mice Thus, injury-induced activation of iNOS requires apoE recruitment. Moreover, both apoE and iNOS are necessary for suppression of cell proliferation, and apoE recruitment without iNOS expression resulted in medial smooth muscle hyperplasia without their migration to the intima.


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