Key result
VEGF-A increases pulmonary valve endothelial cell migration via NFATc1 activation, with DSCR1 silencing increasing and HB-EGF silencing inhibiting migration.
The VEGF-A/NFATc1 signaling pathway differentially regulates pulmonary valve endothelial cell migration through downstream genes DSCR1 and HB-EGF, which may be crucial for post-natal valvular repair.
Should not change practice; hypothesis-generating for VEGF-A/NFATc1 in post-natal valvular repair.
We have reported that vascular endothelial growth factor (VEGF)-A induces the proliferation of human pulmonary valve endothelial cells (HPVECs) through nuclear factor in activated T cells (NFAT)c1 activation. Here we show that VEGF-A increases the migration of HPVECs through NFATc1 activation, suggesting that VEGF-A/NFATc1 regulates the migration of HPVECs. To learn how this pathway may be involved in post-natal valvular repair, HPVECs were treated with VEGF-A, with or without cyclosporine A to selectively block VEGF-NFATc1 signaling. Down Syndrome critical region 1 (DSCR1) and heparin-binding EGF-like growth factor (HB-EGF) are two genes identified by DNA microarray as being up-regulated by VEGF-A in a cyclosporine-A-sensitive manner. DSCR1 silencing increased the migration of ovine valve endothelial cells, whereas HB-EGF silencing inhibited migration. This differential effect suggests that VEGF-A/NFATc1 signaling might be a crucial coordinator of endothelial cell migration in post-natal valves.
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Jang et al. (2009) studied this question. VEGF-A with or without cyclosporine A / Gene silencing was evaluated on Endothelial cell migration. VEGF-A increases pulmonary valve endothelial cell migration via NFATc1 activation, with DSCR1 silencing increasing and HB-EGF silencing inhibiting migration.
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