Biochemical and functional characterization of nitric oxide synthase III gene transfer using a replication-deficient adenoviral vector

Frey, Armin; Schneider-Rasp, Sonja; Marienfeld, Uta; Yu, Julie C.M.; Paul, Martin; Poller, Wolfgang; Schmidt, Harald

doi:10.1016/s0006-2952(99)00196-3

Cited by 14 publications

(9 citation statements)

References 39 publications

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“…eNOS transfection has an antiatherosclerotic effect even in cases of advanced atherosclerosis, and the administration of L-arginine with the gene transfer of eNOS enhances the effect of eNOS transfection (27,28). We showed that the coadministration of antioxidants with L-arginine and L-citrulline produces an enhanced antiatherosclerotic response in advanced atherosclerosis (29).…”

Section: Discussionmentioning

confidence: 80%

Endothelial cellular senescence is inhibited by nitric oxide: Implications in atherosclerosis associated with menopause and diabetes

Hayashi

Matsui-Hirai

Miyazaki-Akita

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

195

170

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Section: Discussionmentioning

confidence: 80%

Endothelial cellular senescence is inhibited by nitric oxide: Implications in atherosclerosis associated with menopause and diabetes

Hayashi

Matsui-Hirai

Miyazaki-Akita

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

195

170

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“…eNOS activity was determined in homogenates of Sf9 cells (derived from Spodoptera frugiperda ) transfected with a recombinant baculoviral vector expressing human eNOS (Schmidt et al ., 1996; Frey et al ., 1999). A colorimetric 96‐well microtiter plate assay for the determination of enzymatically formed citrulline was performed according to the method of Knipp and Vasak (2000) with slight modifications.…”

Section: Methodsmentioning

confidence: 99%

Comparative pharmacology of chemically distinct NADPH oxidase inhibitors

Wind

Beuerlein

Eucker

et al. 2010

British J Pharmacology

224

191

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BACKGROUND AND PURPOSE Oxidative stress [i.e. increased levels of reactive oxygen species (ROS)] has been suggested as a pathomechanism of different diseases, although the disease‐relevant sources of ROS remain to be identified. One of these sources may be NADPH oxidases. However, due to increasing concerns about the specificity of the compounds commonly used as NADPH oxidase inhibitors, data obtained with these compounds may have to be re‐interpreted. EXPERIMENTAL APPROACH We compared the pharmacological profiles of the commonly used NADPH oxidase inhibitors, diphenylene iodonium (DPI), apocynin and 4‐(2‐amino‐ethyl)‐benzolsulphonyl‐fluoride (AEBSF), as well as the novel triazolo pyrimidine VAS3947. We used several assays for detecting cellular and tissue ROS, as none of them is specific and artefact free. KEY RESULTS DPI abolished NADPH oxidase‐mediated ROS formation, but also inhibited other flavo‐enzymes such as NO synthase (NOS) and xanthine oxidase (XOD). Apocynin interfered with ROS detection and varied considerably in efficacy and potency, as did AEBSF. Conversely, the novel NADPH oxidase inhibitor, VAS3947, consistently inhibited NADPH oxidase activity in low micromolar concentrations, and interfered neither with ROS detection nor with XOD or eNOS activities. VAS3947 attenuated ROS formation in aortas of spontaneously hypertensive rats (SHRs), where NOS or XOD inhibitors were without effect. CONCLUSIONS AND IMPLICATIONS Our data suggest that triazolo pyrimidines such as VAS3947 are specific NADPH oxidase inhibitors, while DPI and apocynin can no longer be recommended. Based on the effects of VAS3947, NADPH oxidases appear to be a major source of ROS in aortas of SHRs.

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“…To prevent intimal hyperplasia caused by impaired NO production, vein grafts co-transduced with NOS2 (inducible NOS) and GTP-CHI were engineered that produced maximal NO levels persisting for more than 10 days [52]. No such cotransduction strategy has yet been attempted for transducing NOS1 (neuronal NOS) or NOS3 (endothelial NOS) to human vascular smooth muscle and human endothelial cells, respectively [53,54]. However, also in this case cotransduction with GTP-CHI might be beneficial since NOS3 expressed by human endothelial cells at physiological levels is not saturated with H 4 -biopterin [55].…”

Section: H 4 -Biopterin Deficiencies and Gene Therapymentioning

confidence: 99%

Tetrahydrobiopterin Biosynthesis, Utilization and Pharmacological Effects

Werner-Felmayer

Golderer²,

Werner

2002

CDM

156

138

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Tetrahydrobiopterin (H4-biopterin) is an essential cofactor of a set of enzymes that are of central metabolic importance, i.e. the hydroxylases of the three aromatic amino acids phenylalanine, tyrosine, and tryptophan, of ether lipid oxidase, and of the three nitric oxide synthase (NOS) isoenzymes. As a consequence, H4-biopterin plays a key role in a vast number of biological processes and pathological states associated with neurotransmitter formation, vasorelaxation, and immune response. In mammals, its biosynthesis is controlled by hormones, cytokines and certain immune stimuli. This review aims to summarize recent developments concerning regulation of H4-biopterin biosynthetic and regulatory enzymes and pharmacological effects of H4-biopterin in various conditions, e.g. endothelial dysfunction or apoptosis of neuronal cells. Also, approaches towards gene therapy of diseases like the different forms of phenylketonuria or of Parkinson's disease are reviewed. Additional emphasis is given to H4-biopterin biosynthesis and function in non-mammalian species such as fruit fly, zebra fish, fungi, slime molds, the bacterium Nocardia as well as to the parasitic protozoan genus of Leishmania that is not capable of pteridine biosynthesis but has evolved a sophisticated salvage network for scavenging various pteridine compounds, notably folate and biopterin.

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Biochemical and functional characterization of nitric oxide synthase III gene transfer using a replication-deficient adenoviral vector

Cited by 14 publications

References 39 publications

Endothelial cellular senescence is inhibited by nitric oxide: Implications in atherosclerosis associated with menopause and diabetes

Endothelial cellular senescence is inhibited by nitric oxide: Implications in atherosclerosis associated with menopause and diabetes

Comparative pharmacology of chemically distinct NADPH oxidase inhibitors

Tetrahydrobiopterin Biosynthesis, Utilization and Pharmacological Effects

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