Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P39060 (endostatin)
 2,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe the development and optimization of an in vivo angiogenesis assay utilizing gelfoam sponges impregnated with 0.4% agarose and different proangiogenic factors, such as basic fibroblast growth factor (bFGF), vascular epidermal growth factor (VEGF), tumor growth factor-alpha (TGF-alpha), and endothelial growth factor (EGF). The sponges are implanted into the subcutis of mice and harvested after different times. The gelfoam sponges are fixed, sectioned, and stained with fluorescent antibodies against CD31. The median number of CD31+ cells is determined in 10 different 0.159-mm2 fields. Proangiogenic molecules induced significant migration and proliferation of endothelial cells. To demonstrate the utility of this assay for evaluation of an antiangiogenic agent, mice were implanted with gelfoam sponges containing different proangiogenic factors and treated orally with water or PTK 787, a novel tyrosine kinase inhibitor with specific activity against the VEGF-R. PTK 787 significantly inhibited angiogenesis in sponges containing agarose + VEGF but not other proangiogenic molecules. The data show that the implanted gelfoam sponges provide a reliable quantitative assay to study in vivo angiogenesis.
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PMID:Quantitative and qualitative in vivo angiogenesis assay. 1206 42

Angiogenesis inhibition, which has been extensively studied for the treatment of various malignancies, is beginning to emerge as a new potential therapy for proliferative synovitis, particularly rheumatoid arthritis (RA). The rheumatoid pannus, the site of inflammation and joint destruction in the rheumatoid synovium, relies on the development of new vasculature to sustain its growth. A host of mediators have been shown to induce angiogenesis at the site of the inflamed synovium; these include vascular endothelial growth factor, fibroblast growth factor, integrin alpha(V)beta3, angiopoietin, prosta-glandin E1 and prostaglandin E2, and matrix metalloproteinases. In addition, hypoxia at the site of synovial inflammation contributes to angiogenesis stimulation. Several naturally-occurring inhibitors exist, such angiostatin and endostatin. There are a number of drugs undergoing study in the treatment of proliferative synovitis, which capitalise on the correlation between angiogenesis inhibition and the reduction of signs and symptoms of RA. Paclitaxel and an anti-integrin alpha(V)beta3 antibody, LM-609, are currently in clinical trials. Other drugs that may inhibit angiogenesis in RA include TNP-470 (formerly called AGM-1470), PPI-2458, PTK-787, bevacizumab and thalidomide. Many of these drugs have shown promise for the treatment of oncologic disorders, and are now being evaluated for the treatment of proliferative synovitis.
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PMID:New antiangiogenic strategies for the treatment of proliferative synovitis. 1570 17