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Differential functions of genes regulated by VEGF–NFATc1 signaling pathway in the migration of pulmonary valve endothelial cells
Author(s) -
Jang Gun Hyuk,
Park In-Sook,
Yang Jeong Hee,
Bischoff Joyce,
Lee You Mie
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2009.11.031
Subject(s) - nfat , microbiology and biotechnology , vascular endothelial growth factor , gene silencing , growth factor , ctgf , chemistry , biology , cancer research , gene , transcription factor , vegf receptors , biochemistry , receptor
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 [1]. 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.