Nitric oxide, S-nitrosation, and endothelial permeability.
S-Nitrosation is rapidly emerging as a regulatory mechanism in vascular biology, with particular importance in the onset of hyperpermeability induced by pro-inflammatory agents. This review focuses on the role of endothelial nitric oxide synthase (eNOS)-derived nitric oxide (NO) in regulating S-Nitrosation of adherens junction proteins. We discuss evidence for translocation of eNOS, via caveolae, to the cytosol and analyze the significance of eNOS location for S-Nitrosation and onset of endothelial hyperpermeability to macromolecules.
Department of Pharmacology and Physiology, New Jersey Medical School; Rutgers, The State University of New Jersey, Newark, NJ, 07101-1709, U.S.A.
Walter N
WN
Durán
Annie V
AV
Beuve
Fabiola A
FA
Sánchez
D021941:Caveolae / Q000378:metabolism; D003600:Cytosol / Q000378:metabolism; D042783:Endothelial Cells / Q000378:metabolism*; D006801:Humans; D009569:Nitric Oxide / Q000235:genetics / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000235:genetics* / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D015538:Nitrosation / Q000235:genetics; D010539:Permeability
D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III
S-Nitrosation; VE-cadherin; adherens junction proteins; endothelial nitric oxide synthase; endothelial permeability; endothelium; microvascular permeability; nitric oxide; p120-catenin; regulation of inflammatory hyperpermeability