Open AccessOxidized LDL Inhibits Vascular Endothelial Growth Factor–Induced Endothelial Cell Migration by an Inhibitory Effect on the Akt/Endothelial Nitric Oxide Synthase Pathway
Author(s) -
Emmanouil Chavakis,
Elisabeth Dernbach,
Corinna Hermann,
Ulrich F. Mondorf,
Andreas M. Zeiher,
Stefanie Dimmeler
Publication year - 2001
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.103.16.2102
Subject(s) - enos , protein kinase b , dephosphorylation , nitric oxide , nitric oxide synthase type iii , vascular endothelial growth factor , endothelial stem cell , vascular endothelial growth factor a , phosphorylation , nitric oxide synthase , microbiology and biotechnology , medicine , endocrinology , chemistry , biology , biochemistry , in vitro , vegf receptors , phosphatase
Oxidized LDL (oxLDL) inhibits endothelial cell (EC) migration. Stimulating ECs with vascular endothelial growth factor (VEGF) leads to the activation of Akt/protein kinase B, which in turn activates endothelial nitric oxide synthase (eNOS) by phosphorylation on serine 1177. VEGF-induced cell migration is dependent on the generation of nitric oxide (NO). Therefore, we investigated whether oxLDL affects EC migration by an inhibitory effect on the Akt/eNOS pathway.
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