%0 Journal Article %1 Shen.1999 %A Shen, B. Q. %A Lee, D. Y. %A Zioncheck, T. F. %D 1999 %J J.Biol.Chem. %K & A Adrenal Animals Aorta C Cattle Cell Cells Cortex Cultured Endothelial Endothelium Enzyme Enzymologic Ester Expression Factor Factors Gene Growth II Inhibitors Kinase Kinases Line Lymphokines Methyl NG-Nitroarginine Nitric Oxide Penicillamine Pharmacokinetics Protein Protein-Tyrosine Proteins Receptor Receptors Recombinant Regulation Signal Substances Synthase Transduction Type Tyrosine Up-Regulation Vascular analogs cells derivatives drug effects metabolism pharmacology protein %N 46 %P 33057-33063 %T Vascular endothelial growth factor governs endothelial nitric-oxide synthase expression via a KDR/Flk-1 receptor and a protein kinase C signaling pathway %U PM:10551875 %V 274 %X The mechanism by which vascular endothelial growth factor (VEGF) regulates endothelial nitric-oxide synthase (eNOS) expression is presently unclear. Here we report that VEGF treatment of bovine adrenal cortex endothelial cells resulted in a 5-fold increase in both eNOS protein and activity. Endothelial NOS expression was maximal following 2 days of constant VEGF exposure (500 pM) and declined to base-line levels by day 5. The elevated eNOS protein level was sustained over the time course if VEGF was co-incubated with L-N(G)-nitroarginine methyl ester, a competitive eNOS inhibitor. Addition of S-nitroso-N-acetylpenicillamine, a nitric oxide donor, prevented VEGF-induced eNOS up-regulation. These data suggest that nitric oxide participates in a negative feedback mechanism regulating eNOS expression. Various approaches were used to investigate the role of the two high affinity VEGF receptors in eNOS up-regulation. A KDR receptor-selective mutant increased eNOS expression, whereas an Flt-1

@article{Shen.1999, abstract = {The mechanism by which vascular endothelial growth factor (VEGF) regulates endothelial nitric-oxide synthase (eNOS) expression is presently unclear. Here we report that VEGF treatment of bovine adrenal cortex endothelial cells resulted in a 5-fold increase in both eNOS protein and activity. Endothelial NOS expression was maximal following 2 days of constant VEGF exposure (500 pM) and declined to base-line levels by day 5. The elevated eNOS protein level was sustained over the time course if VEGF was co-incubated with L-N(G)-nitroarginine methyl ester, a competitive eNOS inhibitor. Addition of S-nitroso-N-acetylpenicillamine, a nitric oxide donor, prevented VEGF-induced eNOS up-regulation. These data suggest that nitric oxide participates in a negative feedback mechanism regulating eNOS expression. Various approaches were used to investigate the role of the two high affinity VEGF receptors in eNOS up-regulation. A KDR receptor-selective mutant increased eNOS expression, whereas an Flt-1}, added-at = {2010-02-05T11:28:39.000+0100}, author = {Shen, B. Q. and Lee, D. Y. and Zioncheck, T. F.}, biburl = {https://www.bibsonomy.org/bibtex/2938204526bc0b026f9e8e9af0e63c628/kanefendt}, interhash = {7e178191a8a944887f65bc4e485d411e}, intrahash = {938204526bc0b026f9e8e9af0e63c628}, journal = {J.Biol.Chem.}, keywords = {& A Adrenal Animals Aorta C Cattle Cell Cells Cortex Cultured Endothelial Endothelium Enzyme Enzymologic Ester Expression Factor Factors Gene Growth II Inhibitors Kinase Kinases Line Lymphokines Methyl NG-Nitroarginine Nitric Oxide Penicillamine Pharmacokinetics Protein Protein-Tyrosine Proteins Receptor Receptors Recombinant Regulation Signal Substances Synthase Transduction Type Tyrosine Up-Regulation Vascular analogs cells derivatives drug effects metabolism pharmacology protein}, number = 46, pages = {33057-33063}, timestamp = {2010-02-05T11:28:47.000+0100}, title = {Vascular endothelial growth factor governs endothelial nitric-oxide synthase expression via a KDR/Flk-1 receptor and a protein kinase C signaling pathway}, url = {PM:10551875}, volume = 274, year = 1999 }