![]() Reactive oxygen species in the form of hydrogen peroxide are increased in the absence of CD70 expression. Loss of CD70 is associated with decreased expression of endothelial nitric oxide synthase, leading to reduced nitric oxide bioavailability and bioactivity. CD70 overexpression enhanced endothelial wound closure, increased NO levels, and attenuated the reduction in eNOS mRNA induced by TNFα.ĬD70 is a novel regulator of endothelial function and homeostasis. CD70 knockdown reduced levels of the H 2O 2 scavenger catalase by contrast, glutathione peroxidase 1 expression and activity were increased. There was increased expression of NADPH oxidase 1 complex and gp91phox expression of copper/zinc and manganese superoxide dismutases was also elevated. ![]() Following treatment with the thioredoxin inhibitor auranofin or with agonist histamine, intracellular H 2O 2 levels increased up to 80% in the cytosol, plasmalemmal caveolae, and mitochondria. These changes were accompanied by reduced NO bioactivity, increased 3-nitrotyrosine levels, and a decrease in the eNOS binding partner heat shock protein 90. Endothelial cells treated with CD70-directed short-interfering RNA demonstrated impaired wound closure, decreased agonist-stimulated NO levels, and reduced eNOS (endothelial nitric oxide synthase) protein. Customer Service and Ordering InformationĪn unbiased phenome-wide association study demonstrated that polymorphisms in CD70 associate with vascular phenotypes.Stroke: Vascular and Interventional Neurology.Journal of the American Heart Association (JAHA).Circ: Cardiovascular Quality & Outcomes.Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB). ![]()
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