Our Teacher, Efimenko.A

T-cadherin suppresses angiogenesis in vivo by inhibiting migration of endothelial cells. Rubina K, Kalinina N, Potekhina A, Efimenko A, Semina E, Poliakov A, Wilkinson DG, Parfyonova Y, Tkachuk V. Department of Biological and Medical Chemistry, Faculty of Fundamental Medicine, Lomonosov Moscow State University, 31-5, Lomonosovsky av., Moscow, 119192, Russia. rksenia@cardio.ru Our previous studies have revealed the abundant expression of T-cadherin--a glycosylphosphatidylinositol (GPI)-anchored member of cadherin superfamily--in endothelial and mural cells in the heart and vasculature. The upregulation of T-cadherin in vascular proliferative disorders such as atherosclerosis and restenosis suggests the involvement of T-cadherin in vascular growth and remodeling. However, the functional significance of this molecule in the vasculature remains unknown. The effect of T-cadherin on angiogenesis in vivo was evaluated using Matrigel implant model. We demonstrate that T-cadherin overexpression in L929 cells injected in Matrigel inhibits neovascularization of the plug. In vitro T-cadherin inhibits the directional migration of endothelial cells, capillary growth, and tube formation but has no effect on endothelial cell proliferation, adhesion, or apoptosis in vitro. These data suggest that T-cadherin expressed in the stroma could act as a negative guidance cue for the ingrowing blood vessels and thus could have an important potential therapeutic application.