期刊
DEVELOPMENT
卷 145, 期 13, 页码 -出版社
COMPANY BIOLOGISTS LTD
DOI: 10.1242/dev.161182
关键词
Vascular malformations; Cdc42; Cell migration; Endothelial axial polarity; Angiogenesis; Proliferation
资金
- Swedish Cancer Foundation [CAN2015/771]
- Vetenskapsradet [VR2015-00550]
- European Research Council [2011-294556, EU-ERC269073]
- Knut och Alice Wallenbergs Stiftelse [2012.0272]
- Fondation Leducq [14-CVD-02]
- FP7 People: Marie-Curie Actions [317250]
- Wenner-Gren Foundation
- Ministerio de Educacion, Cultura y Deporte [EDU/2934/2009]
- Flemish Government
- Federaal Wetenschapsbeleid [IUAP] [P7/03]
- Agentschap voor Innovatie door Wetenschap en Technologie
- Sundhed og Sygdom, Det Frie Forskningsrad
Formation and homeostasis of the vascular system requires several coordinated cellular functions, but their precise interplay during development and their relative importance for vascular pathologies remain poorly understood. Here, we investigated the endothelial functions regulated by Cdc42 and their in vivo relevance during angiogenic sprouting and vascular morphogenesis in the postnatal mouse retina. We found that Cdc42 is required for endothelial tip cell selection, directed cell migration and filopodia formation, but dispensable for cell proliferation or apoptosis. Although the loss of Cdc42 seems generally compatible with apical-basal polarization and lumen formation in retinal blood vessels, it leads to defective endothelial axial polarization and to the formation of severe vascular malformations in capillaries and veins. Tracking of Cdc42-depleted endothelial cells in mosaic retinas suggests that these capillary-venous malformations arise as a consequence of defective cell migration, when endothelial cells that proliferate at normal rates are unable to re-distribute within the vascular network.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据