S-Nitrosation regulated by eNOS-derived NO is an important mechanism in the onset of endothelial hyperpermeability.
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May support mechanistic studies of vascular permeability; leaves open any clinical relevance or therapeutic targeting.
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.
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Durán et al. (2013) studied this question.
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