Gene interactions and pathways from curated databases and text-mining
Biochem Biophys Res Commun 2011, PMID: 21458418

Effects of retinol binding protein-4 on vascular endothelial cells.

Takebayashi, Kohzo; Sohma, Ryouichi; Aso, Yoshimasa; Inukai, Toshihiko

The study was designed to investigate the effect of retinol binding protein (RBP)-4 on the phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathways, which mediate the effects of insulin in vascular endothelial cells. The effects of RBP4 on nitric oxide (NO) and insulin-stimulated endothelin-1 (ET-1) secretion and on phosphorylation (p) of Akt, endothelial NO synthetase (eNOS), and extracellular signal-regulated kinase (ERK)1/2 were investigated in bovine vascular aortic endothelial cells (BAECs). RBP4 showed an acute vasodilatatory effect on aortic rings of rats within a few minutes. In BAECs, RBP4-treatment for 5min significantly increased NO production, but inhibited insulin-stimulated ET-1 secretion. RBP4-induced NO production was not inhibited by tetraacetoxymethylester (BAPTA-AM), an intracellular calcium chelator, but was completely abolished by wortmannin, a PI3K inhibitor. RBP4 significantly increased p-Akt and p-eNOS production, and significantly inhibited p-ERK1/2 production. Triciribine, an Akt inhibitor, and wortmannin significantly inhibited RBP4-induced p-Akt and p-eNOS production. Inhibition of Akt1 by small interfering RNA decreased p-eNOS production enhanced by RBP4 in human umbilical vein endothelial cells. In conclusion, RBP4 has a robust acute effect of enhancement of NO production via stimulation of part of the PI3K/Akt/eNOS pathway and inhibition of ERK1/2 phosphorylation and insulin-induced ET-1 secretion, probably in the MAPK pathway, which results in vasodilatation.

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Text Mining Data

endothelin-1 (ET-1) → insulin: " The effects of RBP4 on nitric oxide ( NO ) and insulin stimulated endothelin-1 (ET-1) secretion and on phosphorylation ( p ) of Akt, endothelial NO synthetase (eNOS), and extracellular signal regulated kinase ( ERK ) 1/2 were investigated in bovine vascular aortic endothelial cells ( BAECs ) "

Akt → insulin: " The effects of RBP4 on nitric oxide ( NO ) and insulin stimulated endothelin-1 (ET-1) secretion and on phosphorylation ( p ) of Akt , endothelial NO synthetase (eNOS), and extracellular signal regulated kinase ( ERK ) 1/2 were investigated in bovine vascular aortic endothelial cells ( BAECs ) "

endothelial NO synthetase (eNOS) → insulin: " The effects of RBP4 on nitric oxide ( NO ) and insulin stimulated endothelin-1 (ET-1) secretion and on phosphorylation ( p ) of Akt, endothelial NO synthetase (eNOS) , and extracellular signal regulated kinase ( ERK ) 1/2 were investigated in bovine vascular aortic endothelial cells ( BAECs ) "

endothelin-1 (ET-1) — RBP4: " The effects of RBP4 on nitric oxide ( NO ) and insulin stimulated endothelin-1 (ET-1) secretion and on phosphorylation ( p ) of Akt, endothelial NO synthetase (eNOS), and extracellular signal regulated kinase ( ERK ) 1/2 were investigated in bovine vascular aortic endothelial cells ( BAECs ) "

Akt — RBP4: " The effects of RBP4 on nitric oxide ( NO ) and insulin stimulated endothelin-1 (ET-1) secretion and on phosphorylation ( p ) of Akt , endothelial NO synthetase (eNOS), and extracellular signal regulated kinase ( ERK ) 1/2 were investigated in bovine vascular aortic endothelial cells ( BAECs ) "

endothelial NO synthetase (eNOS) — RBP4: " The effects of RBP4 on nitric oxide ( NO ) and insulin stimulated endothelin-1 (ET-1) secretion and on phosphorylation ( p ) of Akt, endothelial NO synthetase (eNOS) , and extracellular signal regulated kinase ( ERK ) 1/2 were investigated in bovine vascular aortic endothelial cells ( BAECs ) "

p-ERK1/2 ⊣ p-Akt: " RBP4 significantly increased p-Akt and p-eNOS production, and significantly inhibited p-ERK1/2 production "

p-ERK1/2 ⊣ p-eNOS: " RBP4 significantly increased p-Akt and p-eNOS production, and significantly inhibited p-ERK1/2 production "

p-ERK1/2 ⊣ RBP4: " RBP4 significantly increased p-Akt and p-eNOS production, and significantly inhibited p-ERK1/2 production "

p-ERK1/2 ⊣ p-Akt: " RBP4 significantly increased p-Akt and p-eNOS production, and significantly inhibited p-ERK1/2 production "

p-ERK1/2 ⊣ p-eNOS: " RBP4 significantly increased p-Akt and p-eNOS production, and significantly inhibited p-ERK1/2 production "

p-ERK1/2 ⊣ RBP4: " RBP4 significantly increased p-Akt and p-eNOS production, and significantly inhibited p-ERK1/2 production "

p-Akt → RBP4: " RBP4 significantly increased p-Akt and p-eNOS production, and significantly inhibited p-ERK1/2 production "

p-eNOS → RBP4: " RBP4 significantly increased p-Akt and p-eNOS production, and significantly inhibited p-ERK1/2 production "

p-Akt → RBP4: " Triciribine, an Akt inhibitor, and wortmannin significantly inhibited RBP4 induced p-Akt and p-eNOS production "

p-eNOS → RBP4: " Triciribine, an Akt inhibitor, and wortmannin significantly inhibited RBP4 induced p-Akt and p-eNOS production "

Manually curated Databases

No curated data.