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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Atypical GPI-Anchored T-Cadherin Stimulates Angiogenesis In Vitro and In Vivo.

OBJECTIVE: T-cadherin ( T-cad) is an atypical GPI-anchored member of the cadherin superfamily. In vascular tissue, T-cad expression is increased during atherosclerosis, restenosis, and tumor neovascularization. In vitro, overexpression and/or homophilic ligation of T-cad on endothelial cells (ECs) facilitates migration, proliferation, and survival. This study investigated T-cad effects on angiogenesis. METHODS AND RESULTS: In vitro, T-cad homophilic ligation induced arrangement of ECs into a capillary-like network in a 2-dimensional model of EC differentiation and stimulated in-gel endothelial sprout outgrowth in an EC spheroid model and a modified Nicosia tissue assay. Sprouting from spheroids composed of adenoviral-infected T-cad overexpressing ECs or T-cad siRNA transfected ECs were significantly increased or reduced, respectively. In vivo, T-cad potentiated VEGF effects on neovascularization in a model of myoblast-mediated gene transfer to mouse skeletal muscle; vessel caliber after co-delivery of T-cad and VEGF was significantly greater than after delivery of VEGF alone. CONCLUSIONS: We unequivocally identify T-cad as a novel modulator of angiogenesis and suggest that this molecule can be exploited as a target for modulation of therapeutic angiogenesis, as well as for prevention of pathological conditions associated with abnormal neovascularization.[1]


  1. Atypical GPI-Anchored T-Cadherin Stimulates Angiogenesis In Vitro and In Vivo. Philippova, M., Banfi, A., Ivanov, D., Gianni-Barrera, R., Allenspach, R., Erne, P., Resink, T. Arterioscler. Thromb. Vasc. Biol. (2006) [Pubmed]
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