Glipizide suppresses embryonic vasculogenesis and angiogenesis through targeting natriuretic peptide receptor A
Glipizide suppresses embryonic vasculogenesis and angiogenesis through targeting natriuretic peptide receptor A
复制标题
格列吡嗪通过靶向利钠肽受体 A 抑制胚胎血管生成和血管生成
DOI：
10.1016/j.yexcr.2015.03.012
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发表时间：
2015-05-01
影响因子：
3.7
通讯作者：
Wang, Lijing
中科院分区：
文献类型：
--
作者：
Gu, Quliang;Wang, Chaojie;Wang, Lijing
Glipizide, a second-generation sulfonylurea, has been widely used for the treatment of type 2 diabetes. However, it is controversial whether or not glipizide would affect angiogenesis or vasculogenesis. In the present study, we used early chick embryo model to investigate the effect of glipizide on angiogenesis and vasculogenesis, which are the two major processes for embryonic vasculature formation as well as tumor neovascularization. We found that Glipizide suppressed both angiogenesis in yolk-sac membrane (YSM) and blood island formation during developmental vasculogenesis. Glipizide did not affect either the process of epithelial to mesenchymal transition (EMT) or mesoderm cell migration. In addition, it did not interfere with separation of smooth muscle cell progenitors from hemangioblasts. Moreover, natriuretic peptide receptor A (NPRA) has been identified as the putative target for glipizide's inhibitory effect on vasculogenesis. When NPRA was overexpressed or activated, blood island formation was reduced. NPRA signaling may play a crucial role in the effect of glipizide on vasculogenesis during early embryonic development (C) 2015 Elsevier Inc. All rights reserved.
