%0 Journal Article %1 Hood.1998 %A Hood, J. D. %A Meininger, C. J. %A Ziche, M. %A Granger, H. J. %D 1998 %J Am.J.Physiol %K A Calcium Capillaries Cells Cultured Dose-Response Drug Endothelial Endothelium Enzymologic Expression Factor Factors Gene Growth Human Humans Lymphokines Microcirculation Nitric Oxide Regulation Relationship Research Synthase Time Up-Regulation Vascular cells drug effects metabolism pharmacology physiology protein %N 3 Pt 2 %P H1054-H1058 %T VEGF upregulates ecNOS message, protein, and NO production in human endothelial cells %U PM:9530221 %V 274 %X Vascular endothelial growth factor (VEGF) is an endothelium-specific secreted protein that potently stimulates vasodilation, microvascular hyperpermeability, and angiogenesis. Nitric oxide (NO) is also reported to modulate vascular tone, permeability, and capillary growth. Therefore, we hypothesized that VEGF might regulate endothelial production of NO. The production of nitrogen oxides by human umbilical vein endothelial cells (HUVECs) was measured after 1, 12, 24, and 48 h of incubation with VEGF. VEGF treatment resulted in both an acute (1 h) and chronic (> 24 h) stimulation of NO production. Furthermore, Western and Northern blotting revealed a VEGF-elicited, dose-dependent increase in the cellular content of endothelial cell nitric oxide synthase (ecNOS) message and protein that may account for the chronic upregulation of NO production elicited by VEGF. Finally, endothelial cells pretreated with VEGF for 24 h and subsequently exposed to A-23187 for 1 h produced NO at approximately

@article{Hood.1998, abstract = {Vascular endothelial growth factor (VEGF) is an endothelium-specific secreted protein that potently stimulates vasodilation, microvascular hyperpermeability, and angiogenesis. Nitric oxide (NO) is also reported to modulate vascular tone, permeability, and capillary growth. Therefore, we hypothesized that VEGF might regulate endothelial production of NO. The production of nitrogen oxides by human umbilical vein endothelial cells (HUVECs) was measured after 1, 12, 24, and 48 h of incubation with VEGF. VEGF treatment resulted in both an acute (1 h) and chronic (> 24 h) stimulation of NO production. Furthermore, Western and Northern blotting revealed a VEGF-elicited, dose-dependent increase in the cellular content of endothelial cell nitric oxide synthase (ecNOS) message and protein that may account for the chronic upregulation of NO production elicited by VEGF. Finally, endothelial cells pretreated with VEGF for 24 h and subsequently exposed to A-23187 for 1 h produced NO at approximately}, added-at = {2010-02-05T11:28:39.000+0100}, author = {Hood, J. D. and Meininger, C. J. and Ziche, M. and Granger, H. J.}, biburl = {https://www.bibsonomy.org/bibtex/2e619d006bfc90bced94ddeca2fcb3daa/kanefendt}, interhash = {7b0c6fb758181207400f25a38ba267c3}, intrahash = {e619d006bfc90bced94ddeca2fcb3daa}, journal = {Am.J.Physiol}, keywords = {A Calcium Capillaries Cells Cultured Dose-Response Drug Endothelial Endothelium Enzymologic Expression Factor Factors Gene Growth Human Humans Lymphokines Microcirculation Nitric Oxide Regulation Relationship Research Synthase Time Up-Regulation Vascular cells drug effects metabolism pharmacology physiology protein}, number = {3 Pt 2}, pages = {H1054-H1058}, timestamp = {2010-02-05T11:28:46.000+0100}, title = {VEGF upregulates ecNOS message, protein, and NO production in human endothelial cells}, url = {PM:9530221}, volume = 274, year = 1998 }