Identification of a regulatory cis-element within the 3′-untranslated region of the murine inducible nitric oxide synthase (iNOS) mRNA; interaction with heterogeneous nuclear ribonucleoproteins I and L and role in the iNOS gene expression

2007 ◽  
Vol 44 (4) ◽  
pp. 434-442 ◽  
Author(s):  
Malin Söderberg ◽  
Françoise Raffalli-Mathieu ◽  
Matti A. Lang
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Untranslated Region ◽  
Inos Mrna ◽  
Cis Element ◽  
Inos Gene ◽  
Heterogeneous Nuclear Ribonucleoproteins ◽  
Oxide Synthase ◽  
Inos Gene Expression ◽  
Inducible Nitric Oxide

scholarly journals Essential amino acid tryptophan inhibits induction of inducible nitric oxide synthase gene expression in interleukin-1β stimulated hepatocytes

2019 ◽  
Vol 2 (7) ◽  
pp. 170
Author(s):  
Takumi Tsuda ◽  
Hirokazu Miki ◽  
Richi Nakatake ◽  
Tatsuma Sakaguchi ◽  
Masahiko Hatta ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Inos Expression ◽  
No Production ◽  
Inos Gene ◽  
Oxide Synthase ◽  
Inos Gene Expression ◽  
Inducible Nitric Oxide

Background/objective: Tryptophan exerts protective effects against a variety of organ inflammation and injury, including liver. However, there are few scientific reports about the mechanisms involved in the action. Pro-inflammatory cytokine interleukin (IL)-1β stimulates the induction of inducible nitric oxide synthase (iNOS) expression and NO production in cultured hepatocytes (“in vitro liver injury model”), and the prevention of iNOS expression and NO production is considered to be an indicator of liver protection. This study aimed to examine whether tryptophan influences the induction of iNOS gene expression and the mechanisms.Methods: Tryptophan was added into primary cultures of rat hepatocytes stimulated by IL-1β. The iNOS induction, NO production and its signaling pathway were analyzed.Results: IL-1β induced iNOS gene expression, which was followed by iNOS expression and NO production. Tryptophan inhibited the expression of iNOS mRNA and protein, and decreased the production of NO. Transfection experiments with iNOS promoter-luciferase constructs revealed that tryptophan reduced the activities of iNOS mRNA synthesis and its stability. Tryptophan blocked two essential signaling pathways, the activation of nuclear factor (NF)-κB and upregulation of type I IL-1receptor (IL-1RI).Conclusions: Results indicate that tryptophan can prevent the NO production by the inhibition of iNOS gene expression, in part through NF-κB activation and IL-1RI upregulation, in inflamed hepatocytes. Tryptophan may be a potential therapeutic treatment in injured organs, including liver.Key words: tryptophan, inducible nitric oxide synthase, nitric oxide, cultured hepatocytes, nuclear factor-κB, type I interleukin-1 receptor

Regulation of inducible nitric oxide synthase gene by interleukin-1 beta in rat vascular endothelial cells

1994 ◽  
Vol 267 (6) ◽  
pp. H2318-H2324 ◽  
Author(s):  
K. Kanno ◽  
Y. Hirata ◽  
T. Imai ◽  
M. Iwashina ◽  
F. Marumo
Keyword(s):  
Nitric Oxide ◽  
Northern Blot ◽  
Northern Blot Analysis ◽  
Inos Mrna ◽  
Tgf Beta ◽  
Inos Gene ◽  
Oxide Synthase ◽  
Beta Dose ◽  
Inos Gene Expression ◽  
Inducible Nitric Oxide

To elucidate the regulation of endothelial inducible nitric oxide synthase (iNOS), we studied the effects of interleukin (IL)-1 beta on production of nitric oxide (NO) and expression of iNOS mRNA and iNOS protein in cultured rat aortic endothelial cells (ECs) by measurement of NO2-/NO3- (NOx) and Northern blot and Western blot analyses. Among several cytokines and bacterial lipopolysaccharide tested, IL-1 beta most effectively stimulated NOx production. IL-1 beta dose and time dependently stimulated NOx production. Northern blot analysis using cDNA for mouse liver iNOS as a probe showed that IL-1 beta induced expression of iNOS mRNA and stimulated NOx production in a dose- and time-dependent manner. Transforming growth factor (TGF)-beta and dexamethasone blocked the IL-1 beta-induced NOx production as well as expression of iNOS mRNA and protein. TGF-beta dose dependently inhibited the IL-1 beta-induced NOx production and iNOS mRNA expression. Northern blot analysis for the decay of the IL-1 beta-induced iNOS mRNA revealed the approximate half-life of 4 h. These data indicate that IL-1 beta induces iNOS gene expression and de novo synthesis of iNOS and subsequent NO generation in vascular endothelium and that TGF-beta and glucocorticoid block iNOS gene expression at the transcriptional level.

scholarly journals Influence of hCG on inducible nitric oxide synthase gene expression in ram testicular arteries

2014 ◽  
Vol 86 (3) ◽  
pp. 183
Author(s):  
Maria Matteo ◽  
Annalisa Rizzo ◽  
Ettore Cicinelli ◽  
Elvira Grandone ◽  
Giuseppe Cardo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Inos Expression ◽  
P Value ◽  
Inos Mrna ◽  
Inos Gene ◽  
Before And After ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide ◽  
Nos Gene

Background. Experimental evidence suggests a relationship between the vasodilatory effect of hCG and the NOS system in the testis. The influence of hCG administration on testicular vascular NOS gene expression has not been fully investigated. Objective: This study aimed to evaluate the presence of the nitric oxide syntheses gene in ram testicular arteries and the influence of hCG administration on its expression. Materials and methods: Both testicular arteries of sixteen rams were extracted before and after i.v. administration of 5000 IU of hCG or placebo. The expression of the iNOS gene was investigated by real time PCR. Data were analyzed by means of Wilcoxon and Mann-Whitney tests. A p value of < 0.05 was considered statistically significant. Results: PCR revealed the presence of iNOS mRNA in all basal samples but the expression of the iNOS gene was significantly reduced in all arteries obtained 24 h after the administration of either hCG or placebo. A significant reduction in the expression of iNOS gene was observed in the testicular arteries extracted after 24 h in both treated and placebo groups. On the other hand hCG stimulation did not significantly influence iNOS expression following its administration compared to a placebo. Conclusion: Ram testicular arteries express the iNOS gene but hCG stimulation did not significantly influence iNOS expression. A significant reduction in the expression of this gene was observed in the testicular arteries extracted after 24 h in both treated and placebo groups, suggesting that iNOS expression on the testicular artery could be influenced by the spermatic vessel ligation of the controlateral testis.

Cytokines activate inducible nitric oxide synthase gene transcription in inner medullary collecting duct cells

1995 ◽  
Vol 268 (4) ◽  
pp. F770-F777 ◽  
Author(s):  
M. G. Mohaupt ◽  
J. Schwobel ◽  
J. L. Elzie ◽  
G. S. Kannan ◽  
B. C. Kone
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Cytokines ◽  
Collecting Duct ◽  
Tnf Alpha ◽  
Inos Mrna ◽  
No Production ◽  
Inos Gene ◽  
Medullary Collecting Duct ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

The effects of lipopolysaccharide (LPS) and/or inflammatory cytokines on the expression of inducible nitric oxide synthase (iNOS) were studied in mIMCD-3 cells, derived from the murine inner medullary collecting duct. Under basal conditions, the production of nitrite, a stable metabolite of NO, was negligible; however, incubation with tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IF-gamma) for 24 h resulted in a 12-fold increase in nitrite synthesis and the appearance of abundant iNOS mRNA and protein. The induction of nitrite production and iNOS mRNA was time dependent, requiring approximately 8 h for expression of significant levels of nitrite or iNOS mRNA. Coincubation with the transcription inhibitor actinomycin D or the translation inhibitor cycloheximide prevented the cytokine induction of iNOS mRNA and NO production, indicating that synthesis of intermediary proteins stimulated transcription of the iNOS gene. Nuclear run-on transcription demonstrated that the iNOS gene was transcriptionally inactive under basal conditions, but was markedly induced by TNF-alpha and IF-gamma. These results indicate that inflammatory cytokines stimulate NO production in mIMCD-3 cells by activating iNOS gene transcription in a process that requires new protein synthesis.

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