Notch regulates the angiogenic response via induction of VEGFR-1.

Yasuhiro Funahashi, Carrie J Shawber, Marina Vorontchikhina, Anshula Sharma, Hasina H Outtz, Jan Kitajewski
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引用次数: 95

Abstract

Notch is a critical regulator of angiogenesis and arterial specification. We show that ectopic expression of activated Notch1 induces endothelial morphogenesis in human umbilical vein endothelial cells (HUVEC) in a VEGFR-1-dependent manner. Notch1-mediated upregulation of VEGFR-1 in HUVEC increased their responsiveness to the VEGFR-1 specific ligand, Placental Growth Factor (PlGF). In mice and human endothelial cells, inhibition of Notch signaling resulted in decreased VEGFR-1 expression during VEGF-A-induced neovascularization. In summary, we show that Notch1 plays a role in endothelial cells by regulating VEGFR-1, a function that may be important for physiological and pathological angiogenesis.

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Notch通过诱导VEGFR-1调节血管生成反应。
Notch是血管生成和动脉规范的关键调节因子。我们发现,激活Notch1的异位表达以vegfr -1依赖的方式诱导人脐静脉内皮细胞(HUVEC)的内皮形态发生。notch1介导的HUVEC中VEGFR-1的上调增加了它们对VEGFR-1特异性配体胎盘生长因子(PlGF)的反应性。在小鼠和人内皮细胞中,抑制Notch信号导致vegf - a诱导的新生血管形成过程中VEGFR-1表达降低。总之,我们发现Notch1通过调节VEGFR-1在内皮细胞中发挥作用,这一功能可能对生理性和病理性血管生成很重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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