mRNA expression of nitric oxide synthase and no production in human monocytes in essential hypertension.

1996 ◽  
Vol 9 (4) ◽  
pp. 32A
Author(s):  
M SCHENA
Keyword(s):  
Nitric Oxide ◽  
Essential Hypertension ◽  
Nitric Oxide Synthase ◽  
Mrna Expression ◽  
No Production ◽  
Human Monocytes ◽  
Oxide Synthase

scholarly journals Effect of mast cell granules on the gene expression of nitric oxide synthase and tumour necrosis factor-α in macrophages

1998 ◽  
Vol 7 (5) ◽  
pp. 355-361 ◽  
Author(s):  
Y. Li ◽  
T. D. Nguyen ◽  
A. C. Stechschulte ◽  
D. J. Stechschulte ◽  
K. N. Dileepan
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Mast Cell ◽  
Nitric Oxide Synthase ◽  
Mrna Expression ◽  
Inos Mrna ◽  
No Production ◽  
Activated Macrophages ◽  
Factor Α ◽  
Oxide Synthase

Previous studies have shown that mast cell granules (MCG) inhibit numerous macrophage functions including tumour cytotoxicity, superoxide and nitric oxide (NO) production, and FCγ2a receptor-mediated phagocytosis. In this study, the effect of MCG on macrophage TNFα and nitric oxide synthase (iNOS) mRNA expression, and the production and fate of TNFα were examined. Upon activation with LPS+IFNγ, macrophages expressed both TNFα and iNOS mRNA and produced both TNFα and NO. Co-incubation of LPS+IFNγ-activated macrophages with MCG resulted in dose-dependent inhibition of iNOS mRNA expression. TNFα production in the activated macrophages was decreased by MCG, which was associated with a reduction in TNFα mRNA expression. MCG were also capable of degrading both macrophage-generated and recombinant TNFα. The direct effect of MCG on TNFα was partially reversed by a mixture of protease inhibitors. These results demonstrate that MCG decrease the production of NO and TNFα by inhibiting macrophage iNOS and TNFα gene expression. Furthermore, MCG post-transcriptionally alter TNFα levels via proteolytic degradation.

Nitric oxide synthase: MRNA expression of different isoforms in human monocytes/macrophages

1994 ◽  
Vol 24 (8) ◽  
pp. 1941-1944 ◽  
Author(s):  
Norbert Reiling ◽  
Artur J. Ulmer ◽  
Michael Duchrow ◽  
Martin Ernst ◽  
Hans-Dieter Flad ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mrna Expression ◽  
Human Monocytes ◽  
Oxide Synthase

scholarly journals Interleukin-4 stimulates cGMP production by IFN-gamma-activated human monocytes. Involvement of the nitric oxide synthase pathway

1994 ◽  
Vol 269 (13) ◽  
pp. 9811-9816
Author(s):  
J.P. Kolb ◽  
N. Paul-Eugene ◽  
C. Damais ◽  
K. Yamaoka ◽  
J.C. Drapier ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Interleukin 4 ◽  
Human Monocytes ◽  
Ifn Gamma ◽  
Cgmp Production ◽  
Oxide Synthase

scholarly journals Effects of chitosan on nitric oxide production and inducible nitric oxide synthase activity and mRNA expression in weaned piglets

2018 ◽  
Vol 60 (No. 8) ◽  
pp. 359-366
Author(s):  
J. Li ◽  
B. Shi ◽  
S. Yan ◽  
L. Jin ◽  
Y. Guo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mrna Expression ◽  
Inducible Nitric Oxide Synthase ◽  
No Production ◽  
Weaned Piglets ◽  
Inos Activity ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

The effects of chitosan on nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) activity and gene expression in vivo or vitro were investigated in weaned piglets. In vivo, 180 weaned piglets were assigned to five dietary treatments with six replicates. The piglets were fed on a basal diet supplemented with 0 (control), 100, 500, 1000, and 2000 mg chitosan/kg feed, respectively. In vitro, the peripheral blood mononuclear cells (PBMCs) from a weaned piglet were cultured respectively with 0 (control), 40, 80, 160, and 320 µg chitosan/ml medium. Results showed that serum NO concentrations on days 14 and 28 and iNOS activity on day 28 were quadratically improved with increasing chitosan dose (P < 0.05). The iNOS mRNA expressions were linearly or quadratically enhanced in the duodenum on day 28, and were improved quadratically in the jejunum on days 14 and 28 and in the ileum on day 28 (P < 0.01). In vitro, the NO concentrations, iNOS activity, and mRNA expression in unstimulated PBMCs were quadratically enhanced by chitosan, but the improvement of NO concentrations and iNOS activity by chitosan were markedly inhibited by N-(3-[aminomethyl] benzyl) acetamidine (1400w) (P < 0.05). Moreover, the increase of NO concentrations, iNOS activity, and mRNA expression in PBMCs induced by lipopolysaccharide (LPS) were suppressed significantly by chitosan (P < 0.05). The results indicated that the NO concentrations, iNOS activity, and mRNA expression in piglets were increased by feeding chitosan in a dose-dependent manner. In addition, chitosan improved the NO production in unstimulated PBMCs but inhibited its production in LPS-induced cells, which exerted bidirectional regulatory effects on the NO production via modulated iNOS activity and mRNA expression.

scholarly journals Protein kinase Cδ regulates endothelial nitric oxide synthase expression via Akt activation and nitric oxide generation

2008 ◽  
Vol 294 (3) ◽  
pp. L582-L591 ◽  
Author(s):  
Neetu Sud ◽  
Stephen Wedgwood ◽  
Stephen M. Black
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Promoter Activity ◽  
Dominant Negative ◽  
No Production ◽  
Enos Expression ◽  
Akt Activation ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

In this study, we explore the roles of the delta isoform of PKC (PKCδ) in the regulation of endothelial nitric oxide synthase (eNOS) activity in pulmonary arterial endothelial cells isolated from fetal lambs (FPAECs). Pharmacological inhibition of PKCδ with either rottlerin or with the peptide, δV1-1, acutely attenuated NO production, and this was associated with a decrease in phosphorylation of eNOS at Ser1177 (S1177). The chronic effects of PKCδ inhibition using either rottlerin or the overexpression of a dominant negative PKCδ mutant included the downregulation of eNOS gene expression that was manifested by a decrease in both eNOS promoter activity and protein expression after 24 h of treatment. We also found that PKCδ inhibition blunted Akt activation as observed by a reduction in phosphorylated Akt at position Ser473. Thus, we conclude that PKCδ is actively involved in the activation of Akt. To determine the effect of Akt on eNOS signaling, we overexpressed a dominant negative mutant of Akt and determined its effect of NO generation, eNOS expression, and phosphorylation of eNOS at S1177. Our results demonstrated that Akt inhibition was associated with decreased NO production that correlated with reduced phosphorylation of eNOS at S1177, and decreased eNOS promoter activity. We next evaluated the effect of endogenously produced NO on eNOS expression by incubating FPAECs with the eNOS inhibitor 2-ethyl-2-thiopseudourea (ETU). ETU significantly inhibited NO production, eNOS promoter activity, and eNOS protein levels. Together, our data indicate involvement of PKCδ-mediated Akt activation and NO generation in maintaining eNOS expression.

scholarly journals Induction of nitric oxide synthesis in J774 cells lowers intracellular glutathione: effect of modulated glutathione redox status on nitric oxide synthase induction

1997 ◽  
Vol 322 (2) ◽  
pp. 477-481 ◽  
Author(s):  
John S. HOTHERSALL ◽  
Fernando Q. CUNHA ◽  
Guy H. NEILD ◽  
Alberto A. NOROHNA-DUTRA
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
De Novo ◽  
Redox Status ◽  
No Production ◽  
Duration Of Treatment ◽  
Intracellular Glutathione ◽  
J774 Cells ◽  
Oxide Synthase ◽  
Glutathione Redox

Under pathological conditions, the induction of nitric oxide synthase (NOS) in macrophages is responsible for NO production to a cytotoxic concentration. We have investigated changes to, and the role of, intracellular glutathione in NO production by the activated murine macrophage cell line J774. Total glutathione concentrations (reduced, GSH, plus the disulphide, GSSG) were decreased to 45% of the control 48 h after cells were activated with bacterial lipopolysaccharide plus interferon γ. This was accompanied by a decrease in the GSH/GSSG ratio from 12:1 to 2:1. The intracellular decrease was not accounted for by either GSH or GSSG efflux; on the contrary, rapid export of glutathione in control cells was abrogated during activation. The loss of intra- and extracellular glutathione indicates either a decrease in synthesis de novo, or an increase in utilization, rather than competition for available NADPH. All changes in activated cells were prevented by pretreatment with the NOS inhibitor l-N-(1-iminoethyl)ornithine. Basal glutathione levels in J774 cells were manipulated by pretreatment with (1) buthionine sulphoximine (glutathione synthase inhibitor), (2) acivicin (γ-glutamyltranspeptidase inhibitor), (3) bromo-octane (glutathione S-transferase substrate) and (4) diamide/zinc (thiol oxidant and glutathione reductase inhibitor). All treatments significantly decreased the output of NO following activation. The degree of inhibition was dependent on (i) duration of treatment prior to activation, (ii) rate of depletion or subsequent recovery and (iii) thiol end product. The level of GSH did not significantly affect the production of NO, after induction of NOS. Thus, glutathione redox status appears to plays an important role in NOS induction during macrophage activation.

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