Cardiovascular failure in mouse embryos deficient in VEGF receptor-3
Cardiovascular failure in mouse embryos deficient in VEGF receptor-3
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DOI：
10.1126/science.282.5390.946
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发表时间：
1998-10-30
期刊：
影响因子：
56.9
通讯作者：
Alitalo, K
中科院分区：
文献类型：
--
作者：
Dumont, DJ;Jussila, L;Alitalo, K
血管内皮生长因子（VEGF）是胚胎血管发育和成人组织血管生成的关键调节因子。与VEGF不同，相关的VEGF-C通过其特异性淋巴管内皮受体VEGFR-3刺激淋巴管的生长。在这里，它表明，有针对性的失活的基因编码VEGFR-3导致有缺陷的血管发育在早期小鼠胚胎。发生了血管发生和血管生成，但大血管变得异常组织，管腔有缺陷，导致心包腔内液体积聚和胚胎第9.5天的心血管衰竭。因此，在淋巴管出现之前，VEGFR-3在胚胎心血管系统的发育中具有重要作用。
Vascular endothelial growth factor (VEGF) is a key regulator of blood vessel development in embryos and angiogenesis in adult tissues. Unlike VEGF, the related VEGF-C stimulates the growth of Lymphatic vessels through its specific Lymphatic endothelial receptor VEGFR-3. Here it is shown that targeted inactivation of the gene encoding VEGFR-3 resulted in defective blood vessel development in early mouse embryos. Vasculogenesis and angiogenesis occurred, but Large vessels became abnormally organized with defective lumens, Leading to fluid accumulation in the pericardial cavity and cardiovascular failure at embryonic day 9.5. Thus, VEGFR-3 has an essential role in the development of the embryonic cardiovascular system before the emergence of the Lymphatic vessels.