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Mediators of Inflammation
Volume 2014, Article ID 316150, 11 pages
http://dx.doi.org/10.1155/2014/316150
Research Article

Active Smoking Increases Microsomal PGE2-Synthase-1/PGE-Receptor-4 Axis in Human Abdominal Aortic Aneurysms

1Angiology, Vascular Biology and Inflammation Laboratory, Institute of Biomedical Research of Hospital Santa Creu i Sant Pau (II-B Sant Pau), 08025 Barcelona, Spain
2Vascular Surgery Department, Institute of Biomedical Research of Hospital Santa Creu i Sant Pau (II-B Sant Pau), 08025 Barcelona, Spain
3Autonomous University of Barcelona, Institute of Biomedical Research of Hospital Santa Creu i Sant Pau (II-B Sant Pau), 08025 Barcelona, Spain

Received 19 January 2014; Accepted 10 April 2014; Published 30 April 2014

Academic Editor: Jonathan Peake

Copyright © 2014 Jaime-Félix Dilmé et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background. The cyclooxygenase- (COX-) 2/microsomal PGE-synthase- (mPGES-) 1/PGE-receptor- (EP-) 4 axis could play a key role in the physiopathology of abdominal aortic aneurysm (AAA) in humans. In this study, we investigated the influence of cardiovascular risk factors on the expression of the pathway in human AAA. Methods. Aortic and plasma samples from patients who underwent AAA repair were collected. Patients were grouped according to risk factors. COX-isoenzymes, mPGES-1, EPs, α-actin, and CD45 and CD68 transcripts levels were quantified by QRT-PCR and plasma metabolites by EIA. Results. Current smoking (CS) patients compared to no-CS had significantly higher local levels of mPGES-1 , EP-4 , and metabolites plasma levels . In the multiple linear regression analysis, these parameters remained significantly enhanced in CS after adding confounding factors. Results from association studies with cell type markers suggested that the increased mPGES-1/EP-4 levels were mainly associated with microvascular endothelial cells. Conclusions. This study shows that elements of the pathway, which play an important role in AAA development, are increased in CS. These results provide insight into the relevance of tobacco smoking in AAA development and reinforce the potential of mPGES-1 and EP-4 as targets for therapy in AAA patients.