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. 2017 Sep 18;8:578. doi: 10.1038/s41467-017-00654-w

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — POFUT1 regulates proliferation and angiogenic functions of precursor cells for coronary artery development. During coronary artery development, coronary angiogenic precursor cells give rise to coronary arterial plexuses in the hypoxic and VEGFA-rich inner myocardium by vasculogenesis. These plexuses then invade and fuse to form coronary arteries in the outer myocardium through arteriogenesis. Proliferation of coronary angiogenic cells during coronary vasculogenesis is modulated by POFUT1/DLL4/NOTCH1/VEGFA/VEGFR2 signaling axis. Deletion of Pofut1 suppresses DLL4/NOTCH1 signaling, which in turn elevates VEGFA/VEGFR2 signaling. Augmented VEGFA/VEGFR2 signaling promotes proliferation and angiogenic functions of coronary precursor cells, resulting in excessive non-functional coronary plexuses, which are unable to mature into coronary arteries