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. 2019 Mar 12;10:224. doi: 10.3389/fphys.2019.00224

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Copyright © 2019 Jauhiainen, Laakkonen, Ketola, Toivanen, Nieminen, Ninchoji, Levonen, Kaikkonen and Ylä-Herttuala.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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FLRT3 was upregulated in HUVECs via vascular endothelial growth factor (VEGFR)-2-dependent pathway. (A,B) Stimulation of HUVECs with different doses of VEGFR-2-binding ligands VEGF-A, VEGF-D^ΔNΔC, VEGF-F and PlGF. qPCR measurement for FLRT3 mRNA was performed with target-specific assay-on-demand. (C) Upregulation of FLRT3 mRNA was a rapid response to VEGF-A (50 ng/ml) stimulation. A significant upregulation of UNC5B mRNA was also seen in VEGF-A-stimulated HUVECs; however, the response was weaker and had a slower kinetics. Expression of FLRT2 was not altered under these conditions. (D) SU1498, an inhibitor of VEGFR-2, abolished the VEGF-A-stimulated induction of FLRT3 mRNA in compared to DMSO-treated control cells. For all experiments, results are presented as mean ± SEM and are representative of 2–3 independent experiments done in triplicates. ^∗∗∗p < 0.001; and ns, non-significant.