S-nitrosation of proteins
نویسندگان
چکیده
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.
منابع مشابه
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عنوان ژورنال:
دوره 1 شماره
صفحات -
تاریخ انتشار 2013