Vascular oxidant stress early after balloon injury: evidence for increased NAD(P)H oxidoreductase activity

Novel NAD(P)H Oxidase Inhibitor Suppresses Angioplasty-Induced Superoxide and Neointimal Hyperplasia of Rat Carotid Artery

“…Moreover, ROS measurements immediately after balloon injury and at 1 day confirmed the elevation of vascular O 2 ·Ϫ , which was blocked by gp91ds-tat, consistent with NAD(P)H oxidase involvement. 18,22 These findings appear to support our hypothesis that a gp91 phox -containing NAD(P)H oxidase is involved in neointimal hyperplasia.We recently reported that gp91ds-tat is able to suppress subcellular oxidase activity and whole aortic O 2 ·Ϫ production. 23 In the present study, we confirmed its ability to suppress O 2 ·Ϫ levels in injured rat CCAs.…”

“…6 -10 One factor stimulated by Ang II that is involved in the process of vascular cell proliferation and neointimal growth appears to be superoxide anion (O 2 ·Ϫ ) derived from vascular NAD(P)H oxidase. 11-17 Neointimal proliferation and stenosis after vascular or endovascular procedures in animal models coincide with elevated levels of reactive oxygen species (ROS) implicated in a variety of growth-related signaling pathways 18,19 and smooth muscle cell and fibroblast proliferation and migration. 20,21 Recent reports have suggested that activation of various isoforms of NAD(P)H oxidase leads to increased O 2 ·Ϫ in the vascular wall in response to injury.…”

“…20,21 Recent reports have suggested that activation of various isoforms of NAD(P)H oxidase leads to increased O 2 ·Ϫ in the vascular wall in response to injury. 18,21,22 However, the lack of specific and effective in vivo inhibitors of NAD(P)H oxidase has prevented determination of the functional involvement of NAD(P)H oxidase in this process. Recently, we reported on a chimeric peptide inhibitor (gp91ds-tat) that interferes with the assembly of vascular NAD(P)H oxidase components, and showed that this chimera abolished Ang II-induced aortic O 2 ·Ϫ generation in vitro and in vivo, whereas its scrambled control did not.…”

c-Src and Smooth Muscle NAD(P)H Oxidase

“…21 Recently, cyclic strain has been shown to cause oxidative stress in vascular cells. [22][23][24] Souza et al elegantly demonstrated rapid and massive increases in NAD(P)H oxidase-derived O 2 Ϫ in response to cyclic stretch 25 and upregulation of nox-1, nox-2, and nox-4 in response to carotid balloon injury suggests that all three nox homologues play a role in this process. 26 In fact, We 27 showed that a NAD(P)H oxidase assembly inhibitor significantly blocked this increase in the rat carotid artery, suggesting activation of de novo NAD(P)H oxidase assembly in response to injury, which is essential to hyperplasia.…”

Red wine polyphenols correct vascular function injured by chronic carbon tetrachloride intoxication

“…Finally, as it is mentioned above, the treatment with CCl 4 was associated with destruction of endothelial integrity and the capacity of functional endothelium was decreased so we can suggest that the release of NO was decreased. Moreover, the injury of endothelial cell lining was reported to be associated with an increased production of oxygenfree radicals (Azevedo et al 2000;Souza et al 2000) which react with NO and decrease its bioavailability. Polyphenols as scavengers of oxygen free-radicals could play a crutial role in prevention of further NO degradation.…”