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首页> 外文期刊>Developmental cell >Selective regulation of arterial branching morphogenesis by synectin
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Selective regulation of arterial branching morphogenesis by synectin

机译：synectin对动脉分支形态发生的选择性调控

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Branching morphogenesis is a key process in the formation of vascular networks. To date, little is known regarding the molecular events regulating this process. We investigated the involvement of synectin in this process. In zebrafish embryos, synectin knockdown resulted in a hypoplastic dorsal aorta and hypobranched, stunted, and thin intersomitic vessels due to impaired migration and proliferation of angioblasts and arterial endothelial cells while not affecting venous development. Synectin(-/-) mice demonstrated decreased body and organ size, reduced numbers of arteries, and an altered pattern of arterial branching in multiple vascular beds while the venous system remained normal. Murine synectin(-/-) primary arterial, but not venous, endothelial cells showed decreased in vitro tube formation, migration, and proliferation and impaired polarization due to abnormal localization of activated Rac1. We conclude that synectin is involved in selective regulation of arterial, but not venous, growth and branching morphogenesis and that Rac1 plays an important role in this process.
机译：分支形态发生是血管网络形成的关键过程。迄今为止，关于调节该过程的分子事件知之甚少。我们调查了synectin在此过程中的参与。在斑马鱼胚胎中，由于血管成纤维细胞和动脉内皮细胞的迁移和增殖受损，同时又不影响静脉发育，因此合连蛋白的敲低导致背主动脉发育不良以及分支分支，发育不良和间质细弱。 Synectin（-/-）小鼠表现出机体和器官大小减少，动脉数目减少以及多张血管床中动脉分支模式的改变，而静脉系统保持正常。鼠synectin（-/-）的主动脉，但不是静脉，内皮细胞显示出体外管的形成，迁移和增殖减少，并且由于活化的Rac1的异常定位而导致极化受损。我们得出结论，Synectin参与了动脉的选择性调节，但不参与静脉的生长和分支形态发生，Rac1在此过程中起着重要作用。

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