Increased secretion of tumor necrosis factor-alpha and interferon-gamma by mononuclear leukocytes in patients with ischemic heart disease. Relevance in superoxide anion generation.

Vaddi, Krishna; Nicolini, Fabio; Mehta, Paulette; Mehta, Jawahar L.

doi:10.1161/01.cir.90.2.694

Cited by 146 publications

(71 citation statements)

References 35 publications

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“…23 This could contribute to the observed increase of XDH/XO in patients with CAD because increased secretion of interferon-␥ by activated T-lymphocytes has been demonstrated in human atherosclerotic arteries. 24 Furthermore, experimental studies support the concept that activation of the renin-angiotensin system may contribute to increased vascular XO activity, because inhibition of XO could markedly improve endothelium-dependent vasodilation in reninangiotensinogen-overexpressing rats. 25 During the past decade, several O 2 ·Ϫ -forming enzyme systems using NAD(P)H as a cofactor have been identified in vascular cells that may contribute to NADPH-dependent O 2 ·Ϫ production, such as the vascular isoforms of the leukocyte NAD(P)H oxidase, 26 XO 27 , cytochrome-P450 28 and the uncoupled NO synthase.…”

Section: Discussionmentioning

confidence: 93%

Electron Spin Resonance Characterization of Vascular Xanthine and NAD(P)H Oxidase Activity in Patients With Coronary Artery Disease

et al. 2003

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Background-Increased inactivation of nitric oxide by superoxide (O 2 ·Ϫ ) contributes to endothelial dysfunction in patients with coronary disease (CAD). We therefore characterized the vascular activities of xanthine oxidase and NAD(P)H oxidase, 2 major O 2 ·Ϫ -producing enzyme systems, and their relationship with flow-dependent, endothelium-mediated vasodilation (FDD) in patients with CAD. Methods and Results-Xanthine-and NAD(P)H-mediated O 2 ·Ϫ formation was determined in coronary arteries from 10 patients with CAD and 10 controls by using electron spin resonance spectroscopy. Furthermore, activity of endothelium-bound xanthine oxidase in vivo and FDD of the radial artery were determined in 21 patients with CAD and 10 controls. FDD was measured before and after infusion of the antioxidant vitamin C (25 mg/min i.a.) to determine the portion of FDD inhibited by radicals. In coronary arteries from patients with CAD, xanthine-and NAD (P) 05).Conclusions-The present study represents the first electron spin resonance measurements of xanthine and NAD(P)H oxidase activity in human coronary arteries and supports the concept that increased activities of both enzymes contribute to increased vascular oxidant stress in patients with CAD. Furthermore, the present study suggests that increased xanthine oxidase activity contributes to endothelial dysfunction in patients with CAD and may thereby promote the atherosclerotic process.

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Section: Discussionmentioning

confidence: 93%

Electron Spin Resonance Characterization of Vascular Xanthine and NAD(P)H Oxidase Activity in Patients With Coronary Artery Disease

et al. 2003

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“…It was reported that antioxidants played a role in HDL cholesterol. 14 Oxidants influence the balance of the coagulation system toward platelet aggregation and thrombus formation. 15 Low HDL cholesterol is a coronary risk factor and may also be a prognostic factor of failed coronary reperfusion therapy.…”

Section: Discussionmentioning

confidence: 99%

Increased plasma thioredoxin in patients with acute myocardial infarction

Soejima

Suefuji

Miyamoto

et al. 2003

Clinical Cardiology

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SummaryBackground and hypothesis: Thioredoxin is an important biomarker for oxidative stress. We investigated whether thioredoxin levels were elevated in patients with acute myocardial infarction (AMI) and were associated with the results of coronary reperfusion.Methods: The present study determined plasma thioredoxin levels in 51 patients with AMI, 30 patients with stable exertional angina (SEA), and 30 patients with chest pain syndrome (CPS). Plasma sampling was performed on admission, at 12 h, 1 week, 2 weeks, and 4 weeks in patients with AMI, and after admission in patients with SEA and CPS.Results: Plasma thioredoxin levels on admission were higher in patients with AMI than in those with SEA and CPS. Plasma thioredoxin levels in patients with AMI were decreased in 12 h without further change thereafter. However, thioredoxin levels in patients with AMI remained higher than in those with SEA. In multivariate analysis, higher levels of thioredoxin on admission were a risk factor for failure in emergent reperfusion therapy in patients with AMI independent of other factors.

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“…The inflammatory status plays key roles in undermining atherosclerotic plaque stability (7,(17)(18)(19), which leads to lifethreatening AcS. Metabolic disorders are closely associated with atherosclerosis inflammation (20).…”

Section: Discussionmentioning

confidence: 99%

Visfatin/PBEF/Nampt induces EMMPRIN and MMP-9 production in macrophages via the NAMPT-MAPK (p38, ERK1/2)-NF-κB signaling pathway

Fan

Meng²,

Wang³

et al. 2011

Int J Mol Med

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Abstract. The adipocytokine visfatin is closely associated with metabolic disorders. This study explored the effects of visfatin on macrophage-induced inflammation in atheroma. The ability of visfatin to enhance extracellular matrix metalloproteinase inducer (EMMPRIN) expression, matrix metalloproteinase-9 (MMP-9) production and enzymatic activity in THP-1 derived macrophages as well as the mechanisms involved were investigated. EMMPRIN and MMP-9 mRNA levels were investigated by RT-PcR. EMMPRIN and MMP-9 protein levels, nuclear factor (NF)-κB -p65 protein levels, peroxisome proliferator-activated receptor γ (PPARγ) protein levels, and mitogen-activated protein kinase (MAPK) phosphorylation were determined by Western blotting. MMP-9 enzymatic activity was assayed by gelatin zymography. Visfatin (50-400 ng/ml) induced EMMPRIN and MMP-9 depending on the dosage used. Visfatin elicited the activation of NF-κB and MAPK (p38, ERK1/2). Exogenous nicotinamide mononucleotide (NMN), the product of nicotinamide phosphoribosyltransferase (NAMPT) activity, mimicked the effects of visfatin on MAPK (p38, ERK1/2)-NF-κB activation and EMMPRIN/MMP-9 induction. Using the p38 inhibitor, SB203580, the ERK1/2 inhibitor Pd98059, the NF-κB inhibitor, pyrrolidine dithiocarbamate and the NAMPT inhibitor FK866, we demonstrated that the visfatin pro-inflammatory action was through the NAMPT-MAPK (p38, ERK1/2)-NF-κB pathway. Furthermore, the visfatin pro-inflammatory action was not prevented by insulin receptor blockade or by a PPARγ agonist. Visfatin did not modulate PPARγ expression. Retinoid X receptor (RXR) agonist suppressed the effects of visfatin on EMMPRIN/MMP-9, NF-κB, but not on MAPK activation. In conclusion, we have demonstrated that visfatin enhances atheroma inflammation through the NAMPT-MAPK (p38, ERK1/2)-NF-κB-EMMPRIN/MMP-9 pathway, a key feature of atherosclerotic diseases linked to metabolic disorders.

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Increased secretion of tumor necrosis factor-alpha and interferon-gamma by mononuclear leukocytes in patients with ischemic heart disease. Relevance in superoxide anion generation.

Cited by 146 publications

References 35 publications

Electron Spin Resonance Characterization of Vascular Xanthine and NAD(P)H Oxidase Activity in Patients With Coronary Artery Disease

Electron Spin Resonance Characterization of Vascular Xanthine and NAD(P)H Oxidase Activity in Patients With Coronary Artery Disease

Increased plasma thioredoxin in patients with acute myocardial infarction

Visfatin/PBEF/Nampt induces EMMPRIN and MMP-9 production in macrophages via the NAMPT-MAPK (p38, ERK1/2)-NF-κB signaling pathway

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