期刊
AMERICAN JOURNAL OF PATHOLOGY
卷 176, 期 5, 页码 2309-2319出版社
ELSEVIER SCIENCE INC
DOI: 10.2353/ajpath.2010.090865
关键词
-
类别
资金
- Ministry of Education, Culture, Sports, Science, and Technology of Japan [17014078]
- Japan Society for the Promotion of Science [21390245]
- Mochida Memorial Foundation
- Takeda Science Foundation
- Uehara Memorial Foundation
- Sumitomo Foundation
- Graduate School of Medical Sciences, Kumamoto University
- Grants-in-Aid for Scientific Research [21390245, 17014078] Funding Source: KAKEN
Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by symmetrical polyarticular synovitis of the diarthrodial joints. Several proinflammatory cytokines derived from both infiltrating inflammatory cells and activated resident cells within the RA joint play a fundamental role in the processes that cause inflammation. However, anticytokine treatment is beneficial but not curative, the effects are only partial, and nonresponses are common Therefore, an effort has been made to identify other key regulators of inflammation in articular structures to develop new therapies to suppress synovial inflammation and joint destruction in RA. Adipose tissue-derived angiopoietin-like protein 2 (Angptl2) activates an inflammatory cascade in endothelial cells and induces chemotaxis of monocytes/macrophages in obesity, resulting in initiation and propagation of inflammation within adipose tissues and obesity-related metabolic diseases. Angptl2 mRNA and protein are abundantly expressed in hyperplastic rheumatoid synovium of RA patients, especially in fibroblast-like and macrophage-like synoviocytes, but not in B and T lymphocytes. Angptl2 concentration in joints of RA patients was also significantly increased in comparison with patients with osteoarthritis, which in comparison with RA represents a significantly lower inflammatory grade form of arthritis. Notably, Angptl2 promoted increased chemotactic activities of CD14(+)CD16(-) monocytes from synovial fluid of RA patients. Therefore, Angptl2 acts as an important rheumatoid synovium-derived inflammatory mediator in RA pathogenesis. (Am J Pathol 2010, 176:2309-2319; DOI: 10.2353/ajpath.2010.090865)
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据