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-1β (IL-1β, 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-1β. The sizes of atherosclerotic lesions at the aortic sinus in apoE-/-/IL-1β-/- mice at 12 and 24 weeks of age showed a significant decrease of approximately 30% compared with apoE-/-/IL-1β+/+ mice, and the percentage of the atherosclerotic area to total area of apoE-/-/IL-1β-/- at 24 weeks of age also showed a significant decrease of about 30% compared with apoE-/-/IL-1β+/+. The mRNA levels of vascular cell adhesion molecule (VCAM)-1 and monocyte chemotactic protein-1 in the apoE-/-/ IL-1β-/- aorta were significantly reduced compared with the apoE-/-/IL-1β+/+. Furthermore, VCAM-1 was also reduced at the protein level in apoE-/-/IL-1β-/- aorta compared with apoE-/-/IL-1β+/+. Conclusions - The lack of IL-1β decreases the severity of atherosclerosis in apoE deficient mice, possibly through increased expressions of VCAM-1 and monocyte chemotactic protein-1 in the aorta.
|Number of pages||5|
|Journal||Arteriosclerosis, thrombosis, and vascular biology|
|Publication status||Published - 01-04-2003|
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine