Human lactoferrin upregulates expression of KDR/Flk‐1 and stimulates VEGF‐A‐mediated endothelial cell proliferation and migration | Zendy

Kim Chan Woo | Zendy; Son Kyung-No | Zendy; Choi Sang-Yun | Zendy; Kim Jiyoung | Zendy

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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.

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