Skip Navigation

Cardiovascular Research 2003 60(1):198-204; doi:10.1016/S0008-6363(03)00464-4
© 2003 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Bea, F.
Right arrow Articles by Rosenfeld, M. E
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bea, F.
Right arrow Articles by Rosenfeld, M. E
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2003, European Society of Cardiology

Chronic inhibition of cyclooxygenase-2 does not alter plaque composition in a mouse model of advanced unstable atherosclerosis

Florian Beaa, Erwin Blessingb, Brian J Bennetta, Cho Chou Kuoa, Lee Ann Campbella, Jörg Kreuzerb and Michael E Rosenfelda,*

aDepartment of Pathobiology and the Interdisciplinary Graduate Program in Nutritional Sciences, University of Washington, Seattle, WA, USA
bInnere Medizin III, Universität Heidelberg, Heidelberg, Germany

*Corresponding author. Department of Pathobiology and the Interdisciplinary Graduate Program in Nutritional Science, P.O. Box 353410, University of Washington, Seattle, WA 98195, USA. Tel.: +1-206-543-1738; fax: +1-206-616-1245.Email address: ssmjm{at}u.washington.edu

Objective: Inflammation contributes to atherosclerotic plaque initiation and progression. Recent studies suggest that anti-inflammatory drugs such as cyclooxygenase-2 (Cox-2) inhibitors have anti-atherogenic effects. The current study was designed to investigate whether administration of a Cox-2 inhibitor to older apolipoprotein E deficient (apo E–/–) mice with established lesions alters the composition and increases the stability of the lesions. Methods and results: The Cox-2 inhibitor Celecoxib was administered in chow to 26-week-old, male, apo E–/– mice exhibiting advanced, unstable atherosclerotic lesions within the innominate/brachiocephalic artery. Mice administered Celecoxib had no significant changes in serum cholesterol or the average cross sectional area of atherosclerotic lesion in the innominate artery after 15 weeks of treatment in comparison to non-treated control mice. Histological analyses of sections of the innominate artery demonstrated no significant changes in the frequency of markers of advanced and unstable atherosclerotic plaques, including intra-plaque hemorrhage, vascular calcification, thinning of the fibrous cap, size of the necrotic core and macrophage content. There were also no significant differences in the content of Cox-2 within the lesions. Quantitative real time polymerase chain reaction with mRNA isolated from the aorta of each mouse revealed no significant changes in the expression of tissue factor and inducible nitric oxide synthase. However, mRNA levels for MCP-1 were increased fivefold following 15 weeks of treatment with Celecoxib in comparison to non-treated control mice. Conclusions: These data suggest that Celecoxib has no effect on the composition of advanced atherosclerotic lesions in older apo E–/– mice.

KEYWORDS Atherosclerosis; Cyclooxygenase-2; Infection/inflammation; Macrophages

Time for primary review 14 days.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.