Internalization of eNOS and NO delivery to subcellular targets determine agonist-induced hyperpermeability

• Published in: Proceedings of the National Academy of Sciences - PNAS Vol. 106; no. 16; pp. 6849 - 6853
• Main Authors: Sánchez, Fabiola A, Rana, Roshniben, Kim, David D, Iwahashi, Toru, Zheng, Ruifang, Lal, Brajesh K, Gordon, Donna M, Meininger, Cynthia J, Durán, Walter N
• Format: Journal Article
• Language: English
• Published: United States National Academy of Sciences 21.04.2009; National Acad Sciences
• Subjects: Animals; Biological Sciences; Capillary Permeability - drug effects; Cattle; Caveolae; Caveolae - drug effects; Caveolae - metabolism; Cell membranes; Complex Systems: From Chemistry to Systems Biology Special Feature; Cyclodextrins; Endocytosis; Endocytosis - drug effects; Endothelial cells; Endothelial Cells - cytology; Endothelial Cells - drug effects; Endothelial Cells - enzymology; Enzyme Activation - drug effects; Internalization; Membranes; Molecular biology; Mutation; Nitric oxide; Nitric Oxide - metabolism; Nitric Oxide Synthase Type III - metabolism; Oxides; Phosphorylation; Physiological regulation; Plasma; Platelet Activating Factor - pharmacology; Recombinant Fusion Proteins - metabolism; Subcellular Fractions - drug effects; Subcellular Fractions - enzymology; Transfection; Vascular Endothelial Growth Factor A - pharmacology

The molecular mechanisms of endothelial nitric oxide synthase (eNOS) regulation of microvascular permeability remain unresolved. Agonist-induced internalization may have a role in this process. We demonstrate here that internalization of eNOS is required to deliver NO to subcellular locations to inc...