Journal
BIOCHEMICAL JOURNAL
Volume 374, Issue -, Pages 63-69Publisher
PORTLAND PRESS LTD
DOI: 10.1042/BJ20030326
Keywords
hepatocyte growth factor (HGF); mitogen-activated protein kinase; nitric oxide; nitric oxide synthase; wortmannin
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Hepatocyte growth factor (HGF) causes endothelium-dependent vasodilation, but its relation to endothelial nitric oxide synthase (eNOS) activity remains to be elucidated. Treatment of bovine aortic endothelial cells with HGF increased eNOS activity within minutes, accompanied by an increase of activity-related site-specific phosphorylation of eNOS. The phosphorylation was completely abolished by pretreatment of the cells with a phosphoinositide 3-kinase (PI3K) inhibitor (wortmannin) and by transfection of dominant-negative Akt, and the enzyme activity was inhibited by wortmannin. In addition, eNOS activity and phos phorylation were abolished by pretreatment of the cells with an intracellular Ca2+-chelator, bis-(o-aminophenoxy)ethane-N,N, N',N'-tetra-acetic acid tetrakis(acetoxymethyl ester) (BAPTA/ AM), with a suppression of Akt phosphorylation. These results suggest that HGF stimulates eNOS activity by a PI3K/Akt-dependent phosphorylation in a Ca2+ -sensitive manner in vascular endothelial cells.
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