on February 27, 2003
Arteriosclerosis, Thrombosis, and Vascular Biology. 2003
Published online before print February 27, 2003, doi: 10.1161/01.ATV.0000064374.15232.C3
Published online before print February 27, 2003, doi: 10.1161/01.ATV.0000064374.15232.C3
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Submitted on November 19, 2002
Accepted on February 6, 2003
Lack of Interleukin-1
Decreases the Severity of Atherosclerosis in ApoE-Deficient Mice
Hirokazu Kirii ;
From the Department of Clinical Laboratory Medicine (H.K., T.N., Y.Y., H.W., K.S., M.S.) and First Department of Internal Medicine (H.K., H.M.), Gifu University School of Medicine; Institute of Medical Science (Y.I.), University of Tokyo; and Institute of Laboratory Animals (M.A.), Kanazawa University School of Medicine, Japan.
* To whom correspondence should be addressed. E-mail: seishima{at}cc.gifu-u.ac.jp.
Objective--Atherosclerosis is considered to be a chronic inflammatory disease and many cytokines participate in the development of atherosclerosis. We focused on the role of interleukin-1
(IL-1), one of the proinflammatory cytokines secreted by monocytes/macrophages, in the progression of atherosclerosis.
Methods and Results--We generated mice lacking both apoE and IL-1. The sizes of atherosclerotic lesions at the aortic sinus in apoE-/-/IL-1-/-mice at 12 and 24 weeks of age showed a significant decrease of approximately 30% compared with apoE-/-/IL-1+/+ mice, and the percentage of the atherosclerotic area to total area of apoE-/-/IL-1-/- at 24 weeks of age also showed a significant decrease of about 30% compared with apoE-/-/IL-1+/+. The mRNA levels of vascular cell adhesion molecule (VCAM)-1 and monocyte chemotactic protein-1 in the apoE-/-/IL-1-/- aorta were significantly reduced compared with the apoE-/-/IL-1+/+. Furthermore, VCAM-1 was also reduced at the protein level in apoE-/-/IL-1-/- aorta compared with apoE-/-/IL-1+/+.
Conclusions--The lack of IL-1 decreases the severity of atherosclerosis in apoE deficient mice, possibly through increased expressions of VCAM-1 and monocyte chemotactic protein-1 in the aorta.
Key words: interleukin-1
•
atherosclerosis •
vascular cell adhesion molecule-1 •
monocyte chemotactic protein-1
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