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4 results on '"De Cristofaro, F"'

1. Nitric oxide prevents inducible cyclooxygenase expression by inhibiting nuclear factor-kappa B and nuclear factor-interleukin-6 activation.

Author

D'Acquisto F, Maiuri MC, de Cristofaro F, and Carnuccio R

Subjects
Animals, CCAAT-Enhancer-Binding Protein-beta metabolism, Cell Line, Cyclooxygenase 2, Cyclooxygenase 2 Inhibitors, Dinoprostone metabolism, Dose-Response Relationship, Drug, Down-Regulation drug effects, Down-Regulation physiology, Enzyme Induction drug effects, Enzyme Induction physiology, Isoenzymes metabolism, Lipopolysaccharides pharmacology, Macrophages drug effects, Macrophages enzymology, Macrophages metabolism, Mice, NF-kappa B metabolism, Nitric Oxide Donors pharmacology, Prostaglandin-Endoperoxide Synthases metabolism, CCAAT-Enhancer-Binding Protein-beta antagonists & inhibitors, Cyclooxygenase Inhibitors pharmacology, NF-kappa B antagonists & inhibitors, Nitric Oxide physiology, Prostaglandin-Endoperoxide Synthases biosynthesis
Abstract

Stimulation of J774 macrophages with lipopolysaccharide (LPS) leads to the release of large amounts of prostaglandins (PGs) generated by the inducible isoform of cyclooxygenase (COX-2). Nitric oxide (NO), a pleiotropic free radical, has been demonstrated to modulate the release of a broad range of inflammatory mediators, amongst these PGs. In the present study we investigated the molecular mechanism by which NO affects cyclooxygenase pathway. Incubation of J774 cells with LPS caused an increase of prostaglandin E2 production and COX-2 protein expression which was prevented in a concentration-dependent fashion by pre-incubating cells with sodium nitroprusside (SNP) and S-nitroso-glutathione (GSNO), two NO-generating agents. Electrophoretic mobility shift assay indicated that both NO-generating agents blocked LPS-induced activation of nuclear factor-kappaB (NF-kappaB) by increasing IkappaB-alpha protein expression and blocking nuclear translocation of NF-kappaB subunits p50 and p65. SNP and GSNO also inhibited nuclear factor-interleukin-6 (NF-IL6) activation. These results show for the first time that SNP and GSNO down-regulate LPS-induced COX-2 expression by inhibiting NF-kappaB and NF-IL6 activation and suggest a negative feed-back mechanism that may be important for limiting excessive or prolonged PGs production in pathological events.

Published
2001
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2. Protective role of nuclear factor kappa B against nitric oxide-induced apoptosis in J774 macrophages.

Author

D'Acquisto F, de Cristofaro F, Maiuri MC, Tajana G, and Carnuccio R

Subjects
Amino Acid Chloromethyl Ketones pharmacology, Animals, Cell Line metabolism, Cell Survival drug effects, DNA Fragmentation drug effects, DNA Fragmentation physiology, DNA-Binding Proteins drug effects, Mice, NF-KappaB Inhibitor alpha, Nitroprusside pharmacology, Apoptosis physiology, Cell Survival physiology, DNA-Binding Proteins antagonists & inhibitors, I-kappa B Proteins, Macrophages physiology, NF-kappa B physiology, Nitric Oxide metabolism
Abstract

We investigated the role of constitutive transcription factor nuclear factor kappaB (NF-kappaB) in nitric oxide (NO)-mediated apoptosis in J774 macrophages. Our results show that NF-kappaB is present in untreated J774 cells in a form constitutively active. Incubation of cells with sodium nitroprusside (SNP) and S-nitroso-glutathione (GSNO), two NO-generating compounds, caused: (a) inhibition of constitutive NF-kappaB/DNA binding activity; (b) decrease of cell viability; (c) DNA fragmentation; (d) ApopTag positivity. Pyrrolidine dithiocarbamate (PDTC) and N-alpha-para-tosyl-L-lysine chloromethyl ketone (TLCK), two inhibitors of NF-kappaB activation, showed the same effects of both NO-generating compounds. Furthermore, SNP and GSNO as well as PDTC and TLCK significantly increased the cytoplasmic level of IkappaBalpha. All together these results demonstrate that constitutive NF-kappaB protects J774 macrophages from NO-induced apoptosis. Moreover, these findings show, for the first time, that NO-generating compounds may induce apoptosis in J774 macrophages by down-regulating constitutive NF-kappaB/DNA binding activity and suggest a novel mechanism by which NO induces apoptosis.

Published
2001
Full Text
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3. Nitric oxide prevents inducible cyclooxygenase expression by inhibiting nuclear factor-kappa B and nuclear factor-interleukin-6 activation

Author

Rosa Carnuccio, Maria Chiara Maiuri, Fulvio D'Acquisto, de Cristofaro F, D'Acquisto, F, Maiuri, MARIA CHIARA, DE CRISTOFARO, F, and Carnuccio, Rosa

Subjects
Lipopolysaccharides, Lipopolysaccharide, Down-Regulation, Nitric Oxide, Dinoprostone, Nitric oxide, Cyclooxygenase pathway, Cell Line, chemistry.chemical_compound, Mice, medicine, Animals, Electrophoretic mobility shift assay, Cyclooxygenase Inhibitors, Nitric Oxide Donors, Prostaglandin E2, Interleukin 6, Pharmacology, biology, Cyclooxygenase 2 Inhibitors, Dose-Response Relationship, Drug, CCAAT-Enhancer-Binding Protein-beta, Macrophages, NF-kappa B, General Medicine, Molecular biology, Isoenzymes, chemistry, Cyclooxygenase 2, Prostaglandin-Endoperoxide Synthases, Enzyme Induction, biology.protein, lipids (amino acids, peptides, and proteins), Cyclooxygenase, Sodium nitroprusside, medicine.drug
Abstract

Stimulation of J774 macrophages with lipopolysaccharide (LPS) leads to the release of large amounts of prostaglandins (PGs) generated by the inducible isoform of cyclooxygenase (COX-2). Nitric oxide (NO), a pleiotropic free radical, has been demonstrated to modulate the release of a broad range of inflammatory mediators, amongst these PGs. In the present study we investigated the molecular mechanism by which NO affects cyclooxygenase pathway. Incubation of J774 cells with LPS caused an increase of prostaglandin E2 production and COX-2 protein expression which was prevented in a concentration-dependent fashion by pre-incubating cells with sodium nitroprusside (SNP) and S-nitroso-glutathione (GSNO), two NO-generating agents. Electrophoretic mobility shift assay indicated that both NO-generating agents blocked LPS-induced activation of nuclear factor-kappaB (NF-kappaB) by increasing IkappaB-alpha protein expression and blocking nuclear translocation of NF-kappaB subunits p50 and p65. SNP and GSNO also inhibited nuclear factor-interleukin-6 (NF-IL6) activation. These results show for the first time that SNP and GSNO down-regulate LPS-induced COX-2 expression by inhibiting NF-kappaB and NF-IL6 activation and suggest a negative feed-back mechanism that may be important for limiting excessive or prolonged PGs production in pathological events.

Published
2001

4. Protective role of nuclear factor kappaB against nitric oxide-induced apoptosis in J774 macrophages

Author

Rosa Carnuccio, Fulvio D'Acquisto, G Tajana, F de Cristofaro, Maria Chiara Maiuri, D'Acquisto, F, DE CRISTOFARO, F, Maiuri, MARIA CHIARA, Tajana, G, and Carnuccio, Rosa

Subjects
Nitroprusside, Cell Survival, Apoptosis, DNA Fragmentation, Biology, Nitric Oxide, Amino Acid Chloromethyl Ketones, Cell Line, Nitric oxide, Mice, chemistry.chemical_compound, NF-KappaB Inhibitor alpha, Pyrrolidine dithiocarbamate, medicine, Animals, Viability assay, Molecular Biology, Transcription factor, Macrophages, NF-kappa B, Cell Biology, Molecular biology, DNA-Binding Proteins, chemistry, Cytoplasm, DNA fragmentation, I-kappa B Proteins, Sodium nitroprusside, medicine.drug
Abstract

We investigated the role of constitutive transcription factor nuclear factor kappaB (NF-kappaB) in nitric oxide (NO)-mediated apoptosis in J774 macrophages. Our results show that NF-kappaB is present in untreated J774 cells in a form constitutively active. Incubation of cells with sodium nitroprusside (SNP) and S-nitroso-glutathione (GSNO), two NO-generating compounds, caused: (a) inhibition of constitutive NF-kappaB/DNA binding activity; (b) decrease of cell viability; (c) DNA fragmentation; (d) ApopTag positivity. Pyrrolidine dithiocarbamate (PDTC) and N-alpha-para-tosyl-L-lysine chloromethyl ketone (TLCK), two inhibitors of NF-kappaB activation, showed the same effects of both NO-generating compounds. Furthermore, SNP and GSNO as well as PDTC and TLCK significantly increased the cytoplasmic level of IkappaBalpha. All together these results demonstrate that constitutive NF-kappaB protects J774 macrophages from NO-induced apoptosis. Moreover, these findings show, for the first time, that NO-generating compounds may induce apoptosis in J774 macrophages by down-regulating constitutive NF-kappaB/DNA binding activity and suggest a novel mechanism by which NO induces apoptosis.

Published
2001

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