Key result
Hepatocyte growth factor stimulates eNOS activity by a PI3K/Akt-dependent phosphorylation in a Ca(2+)-sensitive manner in vascular endothelial cells.
HGF stimulates eNOS activity in vascular endothelial cells via a PI3K/Akt-dependent and Ca2+-sensitive phosphorylation pathway.
No immediate clinical implications; extends endothelial signaling insights and leaves open in vivo vascular effects.
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 phosphorylation were abolished by pretreatment of the cells with an intracellular Ca(2+)-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 Ca(2+)-sensitive manner in vascular endothelial cells.
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Makondo et al. (2003) studied this question. Hepatocyte growth factor (HGF) was evaluated on eNOS activity and phosphorylation. Hepatocyte growth factor stimulates eNOS activity by a PI3K/Akt-dependent phosphorylation in a Ca(2+)-sensitive manner in vascular endothelial cells.
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