Angiogenesis inhibition suppresses collagen arthritis.

Angiogenesis inhibition suppresses collagen arthritis.
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DOI:
10.1084/jem.175.4.1135
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发表时间:
1992-04-01
期刊:
The Journal of experimental medicine
影响因子:
--
通讯作者:
Brahn E
Brahn E
中科院分区:
其他
文献类型:
--
作者:
Peacock DJ;Banquerigo ML;Brahn E

文献摘要

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在许多疾病如实体瘤、糖尿病视网膜病变和类风湿关节炎中都可以观察到新生血管。这在大鼠拼贴性关节炎(CIA)中也很明显,这是一种具有类似类风湿关节炎的组织学、临床和影像学表现的动物模型。为了评估血管抑制在CIA中的作用,用II型胶原免疫Louvain大鼠诱导关节炎,然后给药血管生成抑制剂AGM-1470,试图预防关节炎或抑制已建立的疾病。根据临床和放射学标准,AGM-1470可预防CIA并显著抑制已建立的疾病,无免疫抑制证据。对照组踝关节的组织学切片显示血管增生和新生血管形成,而实验动物没有。这是第一次在自身免疫性疾病中研究这种新药,并且可能有必要对这种有前景的化合物在其他可能依赖血管生成的疾病(如类风湿关节炎)中的应用进行进一步的评估。
Neovascularization is observed in a spectrum of diseases such as solid tumors, diabetic retinopathy, and rheumatoid arthritis. It is also evident in rat collage-induced arthritis (CIA), an animal model with histologic, clinical, and radiographic manifestations resembling rheumatoid arthritis. To evaluate the effects of angioinhibition in CIA, Louvain rats were immunized with type II collagen to induce arthritis and then administered an angiogenesis inhibitor, AGM-1470, in an attempt to either prevent arthritis or suppress established disease. Using clinical and radiographic criteria, AGM-1470 prevented CIA and significantly suppressed established disease without evidence of immunosuppression. Histologic sections from control ankle joints manifested pannus and neovascularization, which were absent in experimental animals. This is the first study to investigate this novel agent in an autoimmune disease, and additional evaluation of this promising compound in other diseases that are potentially angiogenesis dependent, such as rheumatoid arthritis, might be warranted.