T-cadherin suppresses angiogenesis in vivo by inhibiting migration of endothelial cells

被引：50

作者：

Rubina K. ^{[1
]}

Kalinina N. ^{[1
]}

Potekhina A.V. ^{[1
]}

Efimenko A. ^{[1
]}

Semina E. ^{[1
]}

Poliakov A. ^{[3
]}

Wilkinson D.G. ^{[3
]}

Parfyonova Y. ^{[2
]}

Tkachuk V. ^{[1
]}

机构：

[1] Department of Biological and Medical Chemistry, Faculty of Fundamental Medicine, Lomonosov Moscow State University, 31-5, Lomonosovsky av.

[2] Angiogenesis Laboratory, Russian Cardiology Research and Production Center, 15A, 3rd Cherepkovskaya str.

[3] Division of Developmental Neurobiology, National Institute for Medical Research, The Ridgeway, Mill Hill

来源：

Angiogenesis | 2007年 / 10卷 / 3期

基金：

俄罗斯基础研究基金会;

关键词：

Angiogenesis; Blood vessels; Cadherin; Endothelial cells; Navigating receptor; Vascular biology;

D O I：

10.1007/s10456-007-9072-2

中图分类号：

学科分类号：

摘要：

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. © 2007 Springer Science + Business Media B.V.

引用

页码：183 / 195

页数：12

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