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Human lactoferrin upregulates expression of KDR/Flk‐1 and stimulates VEGF‐A‐mediated endothelial cell proliferation and migration
Author(s) -
Kim Chan Woo,
Son Kyung-No,
Choi Sang-Yun,
Kim Jiyoung
Publication year - 2006
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.2006.06.091
Subject(s) - angiogenesis , downregulation and upregulation , lactoferrin , mapk/erk pathway , chemistry , cell growth , microbiology and biotechnology , endothelial stem cell , cell migration , vascular endothelial growth factor a , phosphorylation , kinase insert domain receptor , vascular endothelial growth factor , biology , cell , in vitro , cancer research , vegf receptors , biochemistry , gene
Lactoferrin (LF) is a multifunctional iron‐binding glycoprotein, which plays a variety of biological processes including immunity. In this study, we demonstrate that human LF upregulates KDR/Flk‐1 mRNA and protein levels in HUVECs at an optimal concentration of 5 μg/ml, which subsequently promotes the VEGF‐induced proliferation and migration of the endothelial cells. Exposure of HUVECs to LF significantly increased VEGF‐induced ERK MAP kinase phosphorylation. The maximal stimulation of KDR/Flk‐1 expression by LF was correlated with LF‐induced increase in cell proliferation and migration. These findings suggest that LF may stimulate in vivo angiogenesis via upregulation of KDR/Flk‐1 expression in endothelial cells.