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Dual role for TWEAK in angiogenic regulation

Departments of Exploratory Science, Molecular Genetics and Protein Engineering, Biogen Inc., 12 Cambridge Center, Cambridge, Massachusetts 02142, USA

*Author for correspondence (e-mail: Aniela_Jakubowski{at}Biogen.com)

Accepted September 24, 2001

Angiogenic regulators modulate endothelial cell functions, including proliferation, migration, secretion, and adhesion, through their action on endothelial cells or other cell types. TWEAK, a novel member of the tumor necrosis factor family, appears to be a pro-angiogenic agent on the basis of previous studies demonstrating its ability to induce interleukin-8 production by epithelial tumor lines, stimulate proliferation of human vascular cell types and neovascularization in rat corneas. Here, we further characterized the angiogenic potential of TWEAK, revealing a dual role for TWEAK as an angiogenic regulator. We demonstrate that TWEAK is a potent inducer of endothelial cell survival and cooperates with basic fibroblast growth factor to induce the proliferation and migration of human endothelial cells and morphogenesis of capillary lumens. In contrast, TWEAK antagonizes the morphogenic response of endothelial cells to vascular endothelial growth factor (VEGF) without inhibiting VEGF-induced survival or proliferation. Thus, our observations suggest that TWEAK may differentially regulate microvascular growth, remodeling and/or maintenance in vivo, depending upon the angiogenic context.

Key words: TWEAK, Tumor necrosis factor-related, Angiogenesis, Basic fibroblast growth factor, Vascular endothelial growth factor

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