Octamer Binding Protein-1 Is Involved in Inhibition of Inducible Nitric Oxide Synthase Expression by Exogenous Nitric Oxide in Murine Liver Cells

Lee, Bok Soo; Kim, Yong Man; Kang, Hyung Sik; Kim, Hwan Mook; Pyun, Kwang Ho; Choi, In Pyo

doi:10.1093/oxfordjournals.jbchem.a002839

Cited by 15 publications

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“…These results suggest that triptolide inhibits the up-regulation of Oct-1 binding activity induced by LPS and PMA. The Oct-1 binding activity is regulated by protein modification such as phosphorylation or S-nitrosylation (31,43). Our results show that triptolide did not reduce the abundance of Oct-1 protein in the nuclear extract, suggesting that it inhibited Oct-1 binding activity induced by LPS and PMA by blocking Oct-1 protein modification.…”

Section: Discussionmentioning

confidence: 61%

“…Therefore, it was possible that inhibition of NF-B, NF-AT, or AP-1 could play a role in suppressing iNOS transcription. It has been reported that mutation of the Oct-1 binding motif in the murine iNOS promoter completely inhibited iNOS transcription in BNL CL2 cells, whereas alteration of other binding sites had no effect on the promoter activity (27,31). and phorbol 12-myristate 13-acetate (PMA; 10 ng/ml) and in the absence or presence of Tript or Dex at the indicated concentrations.…”

Section: Discussionmentioning

confidence: 99%

“…Since Oct-1 is one of the transcription factors that may regulate iNOS transcription (31)(32)(33), the effect of triptolide on Oct-1 binding activity induced by LPS and PMA was analyzed by EMSA. As shown in Figure 7A, stimulation of NIH3T3 cells with LPS and PMA induced Oct-1 binding activity.…”

Section: Figure 3 Effect Of In Vivo Treatment With Ethyl Acetate (Eamentioning

confidence: 99%

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Triptolide, an active component of the Chinese herbal remedy Tripterygium wilfordii Hook F, inhibits production of nitric oxide by decreasing inducible nitric oxide synthase gene transcription

Wang¹,

Ma²,

Tao³

et al. 2004

Arthritis & Rheumatism

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Objective. The ethyl acetate (EA) extract of Tripterygium wilfordii Hook F (TWHF) and its major active component, triptolide, have been reported to be effective in the treatment of rheumatoid arthritis and other autoimmune inflammatory diseases. Nitric oxide (NO) has been recognized as an important mediator of inflammation. This study was therefore undertaken to examine the effects of the EA extract and triptolide on the production of NO and inducible NO synthase (iNOS) gene expression and transcription in vivo and in vitro.Methods. Peritoneal macrophages from C57BL/6J mice treated orally with the EA extract of TWHF were assayed for NO production and iNOS messenger RNA (mRNA) expression by reverse transcriptase-polymerase chain reaction. The murine fibroblast cell line NIH3T3 was also assessed for NO production and iNOS mRNA expression, as well as for iNOS promoter activation, Oct-1 nuclear binding capacity, and Oct-1 protein content by transient transfection, electrophoretic mobility shift assay, and immunoblotting, respectively.Results. NO production and iNOS mRNA expression by macrophages from C57BL/6J mice immunized with trinitrophenyl-bovine serum albumin in Freund's complete adjuvant were significantly inhibited by oral administration of the EA extract (52.3% and 59.8% of control, respectively, at one-eighth of the dose that is lethal for 50% of the animals [LD 50 ] and 21.0% and 38.1% of control, respectively, at one-fourth the LD 50 ). Moreover, the EA extract and triptolide significantly inhibited NO production in vitro in activated peritoneal macrophages, which reflected a decreased level of iNOS mRNA. Finally, triptolide inhibited promoter activity of the iNOS gene and induction of the activity of the regulator of iNOS transcription, Oct-1.Conclusion. The EA extract of TWHF and triptolide inhibit transcription of the iNOS gene. This may contribute to the antiinflammatory effects of this traditional herbal remedy.

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Section: Discussionmentioning

confidence: 61%

Section: Discussionmentioning

confidence: 99%

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Triptolide, an active component of the Chinese herbal remedy Tripterygium wilfordii Hook F, inhibits production of nitric oxide by decreasing inducible nitric oxide synthase gene transcription

Wang¹,

Ma²,

Tao³

et al. 2004

Arthritis & Rheumatism

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“…In the periods of incubation studied, LA and SA did not affect NF-jB activation but increased iNOS expression after 6 and 12 h, respectively. Other transcriptional factors are involved in iNOS expression, as the octamer factor (Oct) [54,55], signal transducer and activator of transcription-1a (STAT-1a) [56][57][58], cAMP-induced transcription factors such as cAMP-responsive element binding protein (CREB) and CCAAT-enhancer box binding protein (C/EBP) [59,60], and activating protein-1 (AP-1) [61]. SA and LA may have activated one of these transcriptional factors and increased iNOS expression.…”

Section: Discussionmentioning

confidence: 99%

Fatty acid control of nitric oxide production by macrophages

Lima

Scavone

et al. 2006

FEBS Letters

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Modulation of macrophage functions by fatty acids (FA) has been studied by several groups, but the effect of FA on nitric oxide production by macrophages has been poorly examined. In the present study the effect of palmitic, stearic, oleic, linoleic, arachidonic, docosahexaenoic and eicosapentaenoic acids on NF-jB activity and NO production in J774 cells (a murine macrophage cell line) was investigated. All FA tested stimulated NO production at low doses (1-10 lM) and inhibited it at high doses (50-200 lM). An increase of iNOS expression and activity in J774 cells treated with a low concentration of FA (5 lM) was observed. The activity of NF-jB was time-dependently enhanced by the FA treatment. The inhibitory effect of FA on NO production may be due to their cytotoxicity, as observed by loss of membrane integrity and/or increase of DNA fragmentation in cells treated for 48 h with high concentrations. The results indicate that, at low concentrations FA increase NO production by J774 cells, whereas at high concentrations they cause cell death.

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“…To prepare an NF-kB probe, oligonucleotides (59 GGCAACTGGGG ACTCTCCCTTT-39 and 59-GGCAAAGGGAGAGTCCCCAGTT-39) with an NF-kB binding site were labeled using the biotin 39 End DNA labeling kit (Pierce, Rockford, IL) and annealed as reported elsewhere (31). Nuclear extracts (8 mg) were incubated with the biotinylated DNA probe at room temperature for 30 minutes in 50 ng/ml poly (dI.dC), 2.5% glycerol, 5 mM MgCl 2 , 0.05% NP-40, and 20 fmol biotin-EBNA control DNA (Pierce).…”

Section: Electrophoretic Mobility Shift Assaymentioning

confidence: 99%

Cigarette Smoke Synergizes Lipopolysaccharide-Induced InterIeukin-1β and Tumor Necrosis Factor–α Secretion from Macrophages via Substance P–Mediated Nuclear Factor–κB Activation

Xu²,

Lin³

2011

Am J Respir Cell Mol Biol

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A recent study has indicated that alveolar macrophages from smokers incubated with lipopolysaccharide (LPS) secrete much more IL-1b and TNF-a than those from healthy nonsmokers, but the mechanisms underlying this augmented secretion by cigarette smoke (CS) remain unknown. CS and LPS reportedly promote macrophages' secreting substance P (SP) that could up-regulate these cytokines' secretion from macrophages by acting on neurokinin 1 receptor (NK1R). Moreover, NF-kB from macrophages participates in NK1R intracellular signaling and synthesis of these cytokines. The present in vitro study was undertaken to examine whether CS is able to synergize these cytokines' response to LPS in macrophages, and if so, whether an amplified SP secretion is responsible for this synergistic cytokines' response via a NK1R-driven NF-kB pathway. THP-1-derived and MH-S macrophages were exposed to control medium and CS condensate (CSC) without or with LPS. We found that LPS, CSC, and CSC1LPS significantly increased IL1b, TNF-a, and SP secretion and that SP secretion markedly preceded cytokines' secretion. CSC1LPS-induced responses were markedly greater than the sum of the responses to CSC and LPS alone, suggesting a synergistic effect. Blocking NK1R reduced the responses of IL-1b, TNF-a, and NF-kB activation to CSC1LPS by 41, 40, and 46%, respectively. NF-kB inhibitors decreased the CSC1LPS-induced cytokines' responses by 70%. Our findings suggest that CS amplifies the LPS-induced macrophages' secretion of IL-1b and TNF-a through synergizing SP secretion, which activates NF-kB via binding with NK1R.Keywords: cytokines; infection; emphysema; signal pathway of NF-kB IL-1b and TNF-a are important cytokines participating in the pathogenesis of multiple pulmonary diseases, such as pulmonary infection, fibrosis, cancer, and emphysema (1-4). For example, cigarette smoke (CS)-induced emphysema was diminished up to 83% in mice that were null of receptors for IL1b and TNF-a (4). Macrophages are one of the important sources these cytokines (5), especially during infection (6). It was reported that pulmonary infection induced by intratracheal instillation of lipopolysaccharide (LPS) substantially promoted cytokine secretion from macrophages (7). A recent study has further indicated that alveolar macrophages from smokers incubated with LPS secrete much more IL-1b and TNF-a than those from healthy nonsmokers (8). This finding, along with a higher secretion of these cytokines in smokers with pulmonary infection than in those without infection (6), implies a synergistic effect of CS exposure on macrophage secretion of these cytokines induced by LPS. However, the exact mechanisms underlying this CS augmented effect on cytokine secretion have not been investigated.There is evidence demonstrating synergistic impacts of CS on the receptors' expression or mucin secretion. We have observed that alveolar macrophages from mice exposed to CS express more neurokinin 1 receptors (NK1R) in response to substance P (SP) compared with those from control mice (9). Moreo...

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Octamer Binding Protein-1 Is Involved in Inhibition of Inducible Nitric Oxide Synthase Expression by Exogenous Nitric Oxide in Murine Liver Cells

Cited by 15 publications

References 0 publications

Triptolide, an active component of the Chinese herbal remedy Tripterygium wilfordii Hook F, inhibits production of nitric oxide by decreasing inducible nitric oxide synthase gene transcription

Triptolide, an active component of the Chinese herbal remedy Tripterygium wilfordii Hook F, inhibits production of nitric oxide by decreasing inducible nitric oxide synthase gene transcription

Fatty acid control of nitric oxide production by macrophages

Cigarette Smoke Synergizes Lipopolysaccharide-Induced InterIeukin-1β and Tumor Necrosis Factor–α Secretion from Macrophages via Substance P–Mediated Nuclear Factor–κB Activation

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