1] Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul 120-749, Republic of Korea [2] Severance Integrative Research Institute for Cerebral and Cardiovascular Diseases, College of Medicine, Yonsei University, Seoul 120-752, Republic of Korea.
Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul 120-749, Republic of Korea.
Nat Commun. 2015 May 12;6:6943. doi: 10.1038/ncomms7943.
Angiogenesis is regulated by the dynamic interaction between endothelial cells (ECs). Hippo-Yes-associated protein (YAP) signalling has emerged as a key pathway that controls organ size and tissue growth by mediating cell contact inhibition. However, the role of YAP in EC has not been defined yet. Here, we show expression of YAP in the developing front of mouse retinal vessels. YAP subcellular localization, phosphorylation and activity are regulated by VE-cadherin-mediated-EC contacts. This VE-cadherin-dependent YAP phosphorylation requires phosphoinositide 3-kinase-Akt activation. We further identify angiopoietin-2 (ANG-2) as a potential transcriptional target of YAP in regulating angiogenic activity of EC in vitro and in vivo. Overexpression of YAP-active form in EC enhances angiogenic sprouting, and this effect is blocked by ANG-2 depletion or soluble Tie-2 treatment. These findings implicate YAP as a critical regulator in angiogenesis and provide new insights into the mechanism coordinating junctional stability and angiogenic activation of ECs.
血管生成受内皮细胞(ECs)之间的动态相互作用调节。Hippo-Yes 相关蛋白(YAP)信号通路已成为控制器官大小和组织生长的关键途径,通过介导细胞接触抑制来实现。然而,YAP 在 EC 中的作用尚未确定。在这里,我们显示 YAP 在发育中的小鼠视网膜血管前端表达。YAP 的亚细胞定位、磷酸化和活性受 VE-钙粘蛋白介导的 EC 接触调节。这种 VE-钙粘蛋白依赖性 YAP 磷酸化需要磷酸肌醇 3-激酶-Akt 的激活。我们进一步鉴定出血管生成素-2(ANG-2)是 YAP 在体外和体内调节 EC 血管生成活性的潜在转录靶点。在 EC 中转染 YAP 活性形式可增强血管生成芽生,而这种作用可被 ANG-2 耗竭或可溶性 Tie-2 处理所阻断。这些发现表明 YAP 是血管生成的关键调节因子,并为协调 EC 连接稳定性和血管生成激活的机制提供了新的见解。