Effect of Advanced Glycosylation End Products on the Induction of Nitric Oxide Synthase in Murine Macrophages

Rojas, Armando; Caveda, Luis; Romay, Cheyla; López, Ellen D. S.; Valdés, Sandra Emma Carmona; Padrón, Julio Rodríguez; Glaria, L.; Martı́nez, Ofelia; Delgado, René

doi:10.1006/bbrc.1996.1180

Cited by 36 publications

(31 citation statements)

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“…Possibly, there is a NO increase due to high glucose, but later in the time course, because of AGE formation, a NO decrease could be measured. Rojas et al have shown that iNOS induced by LPS and IFN-γ is upregulated in murine macrophages when cells were pretreated with AGEs [29]. Hence, although AGE do appear to have vasoactive properties in the absence of hyperglycemia, study results from Moore et al are inconsistent with substantial NO quenching by AGE [24].…”

Section: Discussionmentioning

confidence: 94%

Advanced glycation end products quench nitric oxide in vitro

Uhlmann

Rezzoug

Friedrichs

et al. 2002

Graefe's Arch Clin Exp Ophthalmol

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Section: Discussionmentioning

confidence: 94%

Advanced glycation end products quench nitric oxide in vitro

Uhlmann

Rezzoug

Friedrichs

et al. 2002

Graefe's Arch Clin Exp Ophthalmol

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“…Many studies have demonstrated that total NO production and iNOS expression are increased in myocytes incubated with cytokines, such as IL-1 , TNF-, interferon-and lipopolysaccharide. 43,44 Up-regulation of IL-1 and TNF-might stimulate the production of iNOS in myocytes and macrophages after ischemia-reperfusion. In the present study, it was not clear whether augmented NADPH oxidase activity was derived from myocardium or from phagocytes that migrated into the myocardium or the extracellular matrix.…”

Section: Discussionmentioning

confidence: 99%

CC Chemokine Receptor-2 Deficiency Attenuates Oxidative Stress and Infarct Size Caused by Myocardial Ischemia-Reperfusion in Mice

Hayasaki

Kaikita

Okuma

et al. 2006

Circ J

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arly coronary reperfusion limits myocardial damage and improves survival after myocardial infarction. However, growing evidence indicates that reperfusion itself can cause damage to the ischemic myocardium; this damage is known as post-ischemic myocardial reperfusion injury. 1 Local and systemic inflammatory reactions play a key role in the extension of myocardial tissue injury and adverse effects during left ventricular (LV) recovery. 2 Some experimental studies have demonstrated the importance of monocyte/macrophage infiltration after myocardial infarction. 3,4 Monocyte chemoattractant protein-1 (MCP-1) belongs to the CC chemokine subfamily with 2 adjacent cysteine residues, and serves as a chemotactic and activating factor for the recruitment of monocytes. 5 MCP-1 is secreted by various types of cells, such as monocytes/macrophages, T lymphocytes, endothelial cells, vascular smooth muscle cells and myocytes. [5][6][7] Many experimental and clinical studies have demonstrated up-regulation of MCP-1 after myocardial infarction, with recruitment of monocytes/macrophages to the ischemic myocardium. 8,9 CC chemokine receptor 2 (CCR2) is a major receptor for MCP-1 and MCP-1 appears to bind solely to CCR2. 5 We have previously reported improvement in LV remodeling after myocardial infarction in mice deficient in the gene encoding CCR2 by inhibiting matrix metalloproteinase (MMP) activity. 10 Recently, Dewald et al also reported that MCP-1 -/-mice attenuated LV remodeling after myocardial ischemia followed by reperfusion. 11 In addition to the effects on MMP activity and the release of pro-inflammatory cytokines, macrophages may cause oxidative stress. 12-14 Increased oxidative stress has been implicated in the cell death associated with cardiovascular diseases including ischemia-reperfusion injury. 15 Macrophages have been shown to produce peroxynitrite (ONOO -), a highly reactive oxygen species that can cause cell injury. 16 Several studies have implicated peroxynitrite as a major cause of injury in the heart subjected to ischemiareperfusion or cytokines. 17,18 However, it is not clear whether the inhibition of the CCR2 pathway may attenuate oxidative stress induced by myocardial ischemia-reperfusion in mice. We hypothesized that the inhibition of the MCP-1/CCR2 pathway may contribute to the attenuation of infarct size after myocardial ischemia-reperfusion via inhibition of macrophage-related oxidative stress and MMP.Thus, the purpose of the present study was to investigate the relationship between the monocytic inflammatory response and myocardial ischemia-reperfusion injury by using mice deficient in the CCR2 gene. Background Monocyte chemoattractant protein-1 (MCP-1) and its major receptor, CC chemokine receptor 2 (CCR2), have been shown to contribute to left ventricular remodeling after myocardial infarction. However, it is unknown whether CCR2 deficiency protects the myocardium after myocardial ischemia-reperfusion. The purpose of the present study was to investigate the effects of CCR2 deficiency on myocardial...

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“…AGEs have been shown to stimulate inducible nitric oxide (NO) synthase (iNOS) expression in endothelial cells (7), mouse macrophages (8), and RAW 264.7 cells (9,10). The high concentrations of NO produced by iNOS may play a role in the development of atherosclerosis (11).…”

mentioning

confidence: 99%

Regulation of Inducible Nitric Oxide Synthase Expression in Advanced Glycation End Product–Stimulated RAW 264.7 Cells

Sumi

Ignarro

2004

Diabetes

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Advanced glycation end products (AGEs) are closely linked to the development of diabetic atherosclerosis. The current study examines the induction of inducible nitric oxide (NO) synthase (iNOS) and heme oxygenase (HO)-1 expression by AGEs, as well as the signaling pathways involved and the interplay between these two enzymes. The stimulation of RAW 264.7 cells with 6.64 or 33.2 g/ml AGEs leads to HO-1 protein expression, iNOS protein expression, and nitrite accumulation. AGEs lead to the phosphorylation of p42/44 and p38 mitogen-activated protein kinase (MAPK). The inhibition of p42/44 MAPK and protein kinase C prevented, whereas inhibition of p38 MAPK augmented, AGE-induced nitrite release and iNOS expression. In contrast, HO-1 expression was downregulated by inhibition of p38 MAPK. Furthermore, the expression of both proteins was prevented by coincubation with acetovanillone (NADPH oxidase inhibitor). AGE-induced iNOS expression was negatively regulated by stimulation of HO-1 expression with cadmium chloride or endogenous NO. Tin-protoporphyrin IX (HO-1 inhibitor) partially reversed the cadmium chloride-mediated downregulation of iNOS expression. The current study demonstrates that multiple signaling molecules are involved in AGE-stimulated iNOS and HO-1 expression. There also exists a downregulation of iNOS by its own product as well as the products of HO-1.

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Effect of Advanced Glycosylation End Products on the Induction of Nitric Oxide Synthase in Murine Macrophages

Cited by 36 publications

References 1 publication

Advanced glycation end products quench nitric oxide in vitro

Advanced glycation end products quench nitric oxide in vitro

CC Chemokine Receptor-2 Deficiency Attenuates Oxidative Stress and Infarct Size Caused by Myocardial Ischemia-Reperfusion in Mice

Regulation of Inducible Nitric Oxide Synthase Expression in Advanced Glycation End Product–Stimulated RAW 264.7 Cells

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