Smoking increases tissue factor expression in atherosclerotic plaques : Implications for plaque thrombogenicity

Smoking increases the risk of atherothrombotic events. To determine whether smoking influences plaque thrombogenicity, we examined the effect of cigarette smoking and aspirin use on tissue factor (TF) expression in atherosclerotic plaques. A total of 23 apoE-/- mice were exposed to cigarette smoke w...

Full description

Saved in:
Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 2000-08, Vol.102 (6), p.602-604
Main Authors: MATETZKY, S, TANI, S, KANGAVARI, S, DIMAYUGA, P, YANO, J, XU, H, CHYU, K.-Y, FISHBEIN, M. C, SHAH, P. K, CERCEK, B
Format: Article
Language:English
Subjects:
Aged
Animals
Aorta - metabolism
Apolipoproteins E - deficiency
Apolipoproteins E - genetics
Arteriosclerosis - metabolism
Arteriosclerosis - pathology
Aspirin - therapeutic use
Atherosclerosis (general aspects, experimental research)
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Carotid Arteries - metabolism
Carotid Arteries - pathology
Carotid Artery Diseases - drug therapy
Carotid Artery Diseases - metabolism
Carotid Artery Diseases - pathology
Female
Humans
Male
Medical sciences
Mice
Mice, Knockout - genetics
Middle Aged
Smoking - adverse effects
Thromboplastin - antagonists & inhibitors
Thromboplastin - metabolism
Thrombosis - etiology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Smoking increases the risk of atherothrombotic events. To determine whether smoking influences plaque thrombogenicity, we examined the effect of cigarette smoking and aspirin use on tissue factor (TF) expression in atherosclerotic plaques. A total of 23 apoE-/- mice were exposed to cigarette smoke with (n=9) or without (n=14) aspirin treatment. Eleven mice who were exposed to filtered room air served as controls. Aortic root plaques of mice exposed to smoke had higher immunoreactivity for TF (14+/-4% versus 6.4+/-3%; P=0.0005), vascular cell adhesion molecule-1 (15+/-4% versus 5+/-2%; P=0.002), and macrophages (16+/-5% versus 6+/-2%; P=0.002) compared with nonsmoking controls. Aspirin treatment attenuated smoking-induced changes in plaque composition. In human plaques obtained by carotid endarterectomy, TF immunoreactivity (8+/-5% versus 2+/-2%; P=0.0002) and activity (P=0. 03) were higher in the plaques from smokers (n=28) than those from nonsmokers (n=28). Aspirin use was associated with reduced TF expression in smokers (9+/-8% versus 3+/-4%; P=0.0017). Our results suggest increased plaque TF expression and thrombogenicity as a novel mechanism for the increased risk of atherothrombotic events in smokers. Treatment with aspirin may reduce TF expression.
ISSN:0009-7322
1524-4539
DOI:10.1161/01.CIR.102.6.602