tempo and diphenyleneiodonium

tempo has been researched along with diphenyleneiodonium* in 2 studies

Other Studies

2 other study(ies) available for tempo and diphenyleneiodonium

ArticleYear
Synthetic smooth muscle cell phenotype is associated with increased nicotinamide adenine dinucleotide phosphate oxidase activity: effect on collagen secretion.
    Journal of vascular surgery, 2006, Volume: 43, Issue:2

    Smooth muscle cells (SMCs) from prosthetic vascular grafts secrete higher levels of collagen than aortic SMCs under basal conditions and during incubation with oxidized low-density lipoprotein. We postulated that reactive oxygen species (ROS) contributed to the observed difference. The objective of this study was to assess the effect of ROS on collagen secretion by aortic and graft SMCs and explore the mechanism involved.. SMCs isolated from canine aorta or Dacron thoracoabdominal grafts were incubated with 6-anilinoquinoline-5,8-quinone (LY83583), an agent that induces superoxide production. Type I collagen in the conditioned medium was measured by enzyme-linked immunosorbent assay, and superoxide anion production was measured by lucigenin assay.. LY83583 stimulated a rapid increase in collagen production by graft SMCs that paralleled the LY83583-induced increase in superoxide production. The increase in both collagen and superoxide was greater in graft SMCs than aortic SMCs. Collagen and superoxide production were inhibited by superoxide scavengers. Nicotinamide adenine dinucleotide phosphate (NADPH) induced significantly more superoxide production by graft SMCs than aortic SMCs, suggesting that the NADPH oxidase system was more active in graft SMCs. NADPH oxidase inhibitors blocked the superoxide and collagen production induced by LY83583.. In SMCs, the synthetic phenotype is associated with increased NADPH oxidase activity and elevated superoxide production in response to an oxidative stress. Superoxide, in turn, leads to increased collagen production.. The inflammatory process after prosthetic vascular graft implantation causes oxidative stress that can stimulate collagen production by graft SMCs, contributing to the progression of intimal hyperplasia. The exaggerated response of graft SMCs to oxidative stress offers a potential target for therapeutic interventions.

    Topics: Aminoquinolines; Animals; Aorta; Blood Vessel Prosthesis; Blood Vessel Prosthesis Implantation; Cells, Cultured; Collagen Type I; Cresols; Cyclic N-Oxides; Dogs; Dose-Response Relationship, Drug; Enzyme Inhibitors; Female; Free Radical Scavengers; Hydralazine; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; NADPH Oxidases; Onium Compounds; Oxidative Stress; Phenotype; Polyethylene Terephthalates; Prosthesis Design; Superoxides; Time Factors; Up-Regulation

2006
Hypertonic induction of COX-2 in collecting duct cells by reactive oxygen species of mitochondrial origin.
    The Journal of biological chemistry, 2005, Oct-14, Volume: 280, Issue:41

    Our previous studies have documented MAPK mediation of the hypertonicity-induced stimulation of COX-2 expression in cultured renal medullary epithelial cells. The present study extends this observation by examining the role of reactive oxygen species (ROSs). ROS levels, determined using dichlorodihydrofluorescence diacetate and cytochrome c, were rapidly and significantly increased following exposure of mIMCD-K2 cells to media made hypertonic by adding NaCl. Hypertonic treatment (550 mosmol/kg) for 16 h induced a 5.6-fold increase in COX-2 protein levels and comparable increases in prostaglandin E(2) release, both of which were completely abolished by the NADPH oxidase inhibitor diphenyleneiodonium (25-50 microM). The general antioxidant N-acetyl-l-cysteine (6 mM), and the superoxide dismutase mimetic TEMPO (2.0 mm) reduced COX-2 levels by 75.6 and 79.8%, respectively. Exposure of mIMCD-K2 cells to exogenous O(2)(-.) generated by the xanthine/xanthine oxidase system mimicked the effect of hypertonicity on COX-2 expression and prostaglandin E(2) release. The increases in phosphorylation of ERK1/2 and p38 were detected 20 min following the hypertonic treatment and were both prevented by N-acetyl-l-cysteine. The increases in ROSs in response to hypertonic treatment were completely blocked by any one of the mitochondrial inhibitors tested, such as rotenone, thenoyltrifluoroacetone, or carbonyl cyanide m-chlorophenylhydrazone, associated with remarkable inhibition of COX-2 expression. In contrast, the increases in ROSs were not significantly altered in IMCD cells deficient in either gp91(phox) or p47(phox), nor were the increases in COX-2 expression. We conclude that ROSs derived from mitochondria, but not NADPH oxidase, mediate the hypertonicity-induced phosphorylation of MAPK and the stimulation of COX-2 expression.

    Topics: Acetylcysteine; Animals; Antioxidants; Blotting, Western; Cells, Cultured; Cyclic N-Oxides; Cyclooxygenase 2; Cytochromes c; Dinoprostone; Fluoresceins; Genes, Dominant; Hydrazones; Kidney; Kidney Tubules, Collecting; MAP Kinase Signaling System; Membrane Glycoproteins; Mice; Mitochondria; Mitogen-Activated Protein Kinase 1; Mitogen-Activated Protein Kinase 3; NADPH Oxidase 2; NADPH Oxidases; Onium Compounds; Osmosis; p38 Mitogen-Activated Protein Kinases; Phosphoproteins; Phosphorylation; Promoter Regions, Genetic; Reactive Oxygen Species; Rotenone; Thenoyltrifluoroacetone; Time Factors; Xanthine; Xanthine Oxidase

2005
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