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Tie2 receptor tyrosine kinase, a major mediator of tumor necrosis factor alpha- induced angiogenesis in rheumatoid arthritis. Paper-10000751. RESULTS: Tie2 was implicated in pathologic angiogenesis. Paper-10000751.
However, the molecular mechanisms promoting angiogenesis in RA are not clearly identified. Paper-10000751.
OBJECTIVE: Rheumatoid arthritis ( RA) is an inflammatory disease and an angiogenic disease. Paper-10000751.
These findings suggest paracrine regulation of angiogenesis between endothelial cells and synoviocytes.
CONCLUSION: This study demonstrates that Tie2 regulates angiogenesis in inflammatory synovium. Paper-10000751.
We observed that Tie2 and Ang1 were elevated in human RA synovium. Paper-10000751.
A novel synovium vascular window model was established to study the role of Tie2 in angiogenesis in vivo. Paper-10000751.
We also showed that Tie2 mediated TNF alpha-induced angiogenesis in a mouse cornea assay. Paper-10000751.
Our objective was to study the role of an endothelium-specific receptor tyrosine kinase, Tie2, in angiogenesis of inflammatory arthritis. Paper-10000751.
Using a novel collagen-induced arthritis synovial window model, we demonstrated that Tie2 signaling regulated arthritis angiogenesis in vivo. Paper-10000751.
Tie2 signaling is an important angiogenic mediator that links the proinflammatory cytokine TNF alpha to pathologic angiogenesis. Paper-10000751.
TNF alpha up-regulates Tie2 in endothelial cells through nuclear factor kappa B, and it up-regulates Ang1 in synoviocytes. Paper-10000751.
Primary cultured endothelial cells and synoviocytes were used to study tumor necrosis factor alpha ( TNF alpha)-induced Tie2 and Ang1 expression. Paper-10000751.
In addition, we observed that TNF alpha can regulate Tie2 activation in multiple ways that may involve interactions between endothelial cells and synoviocytes. Paper-10000751.
METHODS: Expression of Tie2 and its ligand, angiopoietin 1 ( Ang1), in human synovium was examined by immunohistochemistry and Western blot. Paper-10000751.
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