help button home button Am J Pathol ASIP MEMBERSHIP
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Moore, Z. W.Q.
Right arrow Articles by Hui, D. Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Moore, Z. W.Q.
Right arrow Articles by Hui, D. Y.
(American Journal of Pathology. 2004;164:2109-2116.)
© 2004 American Society for Investigative Pathology

Vascular Apolipoprotein E Expression and Recruitment from Circulation to Modulate Smooth Muscle Cell Response to Endothelial Denudation

Zachary W.Q. Moore, Binghua Zhu, David G. Kuhel and David Y. Hui

From the Department of Pathology and Laboratory Medicine, University of Cincinnati, Cincinnati, Ohio

Apolipoprotein E (apoE) has been shown previously to have anti-proliferative and anti-migratory effects on smooth muscle cells in culture. In addition, overexpression of the apoE gene also reduces neointimal hyperplasia in mice after endothelial denudation. In this investigation, immunohistochemical techniques were used to demonstrate that apoE was present in the medial smooth muscle layers of the carotid artery between 1 and 28 days after endothelial cell denudation. Analysis of transgenic mice overexpressing human apoE in the liver revealed that apoE was recruited from the circulation to the injured site of the vessel wall. In situ hybridization using a mouse-specific apoE mRNA probe confirmed that apoE was also synthesized in the carotid artery after endothelial denudation. Interestingly, apoE accumulation in apoE transgenic mice followed a layer-specific pattern, and was inversely associated with smooth muscle {alpha}-actin expression. The vascular accumulation of apoE after endothelial denudation, and its assocation with {alpha}-actin-depleted smooth muscle cells, suggest that apoE inhibition of injury-induced neointimal hyperplasia is not due to the inhibition of injury-induced smooth muscle cell de-differentiation, but is likely a direct effect of apoE on smooth muscle cell migration and proliferation.




This article has been cited by other articles:


Home page
 Circ. Res.Home page
M. Mayr, A. Zampetaki, A. Sidibe, U. Mayr, X. Yin, A. I. De Souza, Y.-L. Chung, B. Madhu, P. H. Quax, Y. Hu, et al.
Proteomic and Metabolomic Analysis of Smooth Muscle Cells Derived From the Arterial Media and Adventitial Progenitors of Apolipoprotein E-Deficient Mice
Circ. Res., May 9, 2008; 102(9): 1046 - 1056.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
Q. Xu, A. Bernardo, D. Walker, T. Kanegawa, R. W. Mahley, and Y. Huang
Profile and Regulation of Apolipoprotein E (ApoE) Expression in the CNS in Mice with Targeting of Green Fluorescent Protein Gene to the ApoE Locus.
J. Neurosci., May 10, 2006; 26(19): 4985 - 4994.
[Abstract] [Full Text] [PDF]

Home page
 J. Lipid Res.Home page
Z. W. Q. Moore and D. Y. Hui
Apolipoprotein E inhibition of vascular hyperplasia and neointima formation requires inducible nitric oxide synthase
J. Lipid Res., October 1, 2005; 46(10): 2083 - 2090.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2004 by the American Society for Investigative Pathology.