Lack of interleukin-1beta decreases the severity of atherosclerosis in ApoE-deficient mice (VSports手机版)
- PMID: 12615675
- DOI: "V体育安卓版" 10.1161/01.ATV.0000064374.15232.C3
Lack of interleukin-1beta decreases the severity of atherosclerosis in ApoE-deficient mice (VSports最新版本)
"VSports注册入口" Abstract
Objective: Atherosclerosis is considered to be a chronic inflammatory disease and many cytokines participate in the development of atherosclerosis VSports手机版. We focused on the role of interleukin-1beta (IL-1beta), 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-1beta V体育安卓版. The sizes of atherosclerotic lesions at the aortic sinus in apoE-/-/IL-1beta-/-mice at 12 and 24 weeks of age showed a significant decrease of approximately 30% compared with apoE-/-/IL-1beta+/+ mice, and the percentage of the atherosclerotic area to total area of apoE-/-/IL-1beta-/- at 24 weeks of age also showed a significant decrease of about 30% compared with apoE-/-/IL-1beta+/+. The mRNA levels of vascular cell adhesion molecule (VCAM)-1 and monocyte chemotactic protein-1 in the apoE-/-/IL-1beta-/- aorta were significantly reduced compared with the apoE-/-/IL-1beta+/+. Furthermore, VCAM-1 was also reduced at the protein level in apoE-/-/IL-1beta-/- aorta compared with apoE-/-/IL-1beta+/+. .
Conclusions: The lack of IL-1beta decreases the severity of atherosclerosis in apoE deficient mice, possibly through increased expressions of VCAM-1 and monocyte chemotactic protein-1 in the aorta. V体育ios版.
Publication types
- "VSports app下载" Actions
- VSports手机版 - Actions
MeSH terms
- "VSports在线直播" Actions
- Actions (VSports最新版本)
- "V体育平台登录" Actions
- Actions (VSports)
- "V体育2025版" Actions
- Actions (VSports app下载)
- "V体育ios版" Actions
- VSports注册入口 - Actions
- V体育官网 - Actions
- Actions (V体育平台登录)
Substances
- Actions (V体育平台登录)
- Actions (VSports)
- VSports最新版本 - Actions
LinkOut - more resources
Full Text Sources
Other Literature Sources
Molecular Biology Databases
Research Materials
"V体育2025版" Miscellaneous
