Critical role of TRPC6 channels in VEGF-mediated angiogenesis
Critical role of TRPC6 channels in VEGF-mediated angiogenesis
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TRPC6 通道在 VEGF 介导的血管生成中的关键作用
DOI：
10.1016/j.canlet.2009.03.023
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发表时间：
2009-09-28
期刊：
影响因子：
9.7
通讯作者：
Wang, Yizheng
中科院分区：
文献类型：
--
作者：
Ge, Ruiliang;Tai, Yilin;Wang, Yizheng
细胞内Ca ~（2+）信号在VEGF介导的血管生成中起关键作用。瞬时受体电位经典（TRPC）通道6，一种Ca 2+渗透性非选择性阳离子通道，可被VEGF激活。在这里，我们报告TRPC 6是VEGF介导的血管生成的重要。通过药理学或遗传学方法抑制人脐静脉内皮细胞（HUVECs）中的TRPC 6可将HUVECs阻滞在G2/M期，并抑制VEGF诱导的HUVECs增殖和管形成。此外，抑制TRPC废除VEGF，但不是FGF诱导的血管生成在鸡胚绒毛尿囊膜。这些结果表明TRPC 6在VEGF介导的血管生成中起重要作用。(C)2009爱思唯尔爱尔兰有限公司保留所有权利。
Intracellular Ca2+ signaling plays critical roles in VEGF-mediated angiogenesis. Transient receptor potential canonical (TRPC) channel 6, a Ca2+-permeable non-selective cation channel, can be activated by VEGF. Here, we report that TRPC6 is important for VEGF-mediated angiogenesis. Inhibition of TRPC6 in human umbilical vein endothelial cells (HUVECs) by pharmacological or genetic approaches arrested HUVECs at G2/M phase and suppressed VEGF-induced HUVEC proliferation and tube formation. Furthermore, inhibition of TRPCs abolished VEGF-, but not FGF-induced angiogenesis in the chick embryo chorioallantoic membrane. These results suggest that TRPC6 plays an important role in VEGF-mediated angiogenesis. (C) 2009 Elsevier Ireland Ltd. All rights reserved.