title: S-nitrosation of proteins: An emergent regulatory mechanism in microvascular permeability and vascular function.
abstract: Nitric oxide (NO) is a key factor in inflammation as it regulates microvascular permeability, leukocyte adhesion and wound healing. This mini-review addresses mainly spatial and temporal requirements of NO regulatory mechanisms, with special emphasis on S-nitrosation. Endothelial nitric oxide synthase (eNOS)-derived NO induces S-nitrosation of p120 and β-catenin, particularly in response to platelet-activating factor (PAF), and through traffic and interactions at the adherens junction promotes endothelial hyperpermeability. S-nitrosation is a determinant in vascular processes such as vasodilation and leukocyte-endothelium interactions. Interestingly, NO decreases leukocytes adhesion to endothelium, but the mechanisms are unknown. Advances in NO molecular biology and regulation may serve as a basis for the development of new therapeutic strategies in the treatment of diseases characterized by inflammation such as ischemia-reperfusion injury, stroke, cancer and atherosclerosis.
authors.affiliation: Instituto de Inmunología; Universidad Austral de Chile; Valdivia, Chile.
authors.forename: Fabiola A
authors.initials: FA
authors.lastname: Sánchez
authors.affiliation: Histología y Patología; Universidad Austral de Chile; Valdivia, Chile.
authors.forename: Ingrid P
authors.initials: IP
authors.lastname: Ehrenfeld
authors.affiliation: Department of Pharmacology and Physiology; New Jersey Medical School; University of Medicine and Dentistry of New Jersey; Newark, NJ USA.
authors.forename: Walter N
authors.initials: WN
authors.lastname: Durán
keywords: S-nitrosation; adherens junction; eNOS; microvascular permeability; nitric oxide