Polyclonal antibody against an inducible form of nitric oxide synthase purified from the liver of rats treated with Propionibacterium acnes and lipopolysaccharide

Ohshima, Hiroshi; Brouet, I.; TIu, Bandaletova; Adachi, H.; Oguchi, Shinobu; Iida, Sachio; Kurashima, Yukiko; Morishita, Yoshiyuki; Sügimura, Takashi; Esumi, Hiroyasu

doi:10.1016/0006-291x(92)90443-o

Cited by 54 publications

(32 citation statements)

References 9 publications

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“…iNOS mRNA was induced also in the heart, muscle and testis, but apparently not in the brain and kidney. Ohshima et al (36) reported that iNOS protein was induced in the liver, lung, and spleen of the rat by administration of Propionibacterium acnes and LPS. Hom et al (37) reported that iNOS mRNA and protein were induced by LPS in many tissues of the rat, including the brain and kidney.…”

Section: Discussionmentioning

confidence: 99%

Coinduction of Nitric Oxide Synthase, Argininosuccinate Synthetase, and Argininosuccinate Lyase in Lipopolysaccharide-treated Rats

Nagasaki

Gotoh

Takeya

et al. 1996

Journal of Biological Chemistry

121

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Nitric oxide (NO) is synthesized from arginine by nitric oxide synthase (NOS), and citrulline which is generated can be recycled to arginine by argininosuccinate synthetase (AS) and argininosuccinate lyase (AL). Rats were injected with bacterial lipopolysaccharide (LPS), and expression of the inducible isoform of NOS (iNOS), AS, and AL was analyzed. In RNA blot analysis, iNOS mRNA was undetectable before the LPS treatment but was induced by LPS in the lung, heart, liver, and spleen, and less strongly in the skeletal muscle and testis. AS mRNA was induced in the lung and spleen, and AL mRNA was weakly induced in these tissues. AS and AL mRNAs were abundant in the control liver and remained unchanged after the treatment. Kinetic studies showed that iNOS mRNA increased rapidly in both spleen and lung, reached a maximum 2-5 h after the treatment, and decreased thereafter. On the other hand, AS mRNA increased more slowly and reached a maximum in 6 -12 h (by about 10-fold in the spleen and 2-fold in the lung). AL mRNA in the spleen and lung increased slowly and remained high up to 24 h. In immunoblot analysis, increase of iNOS protein was evident in the lung, liver, and spleen, and there was an increase of AS protein in the lung and spleen. In immunohistochemical analysis, macrophages in the spleen that were negative for iNOS and AS before LPS treatment were strongly positive for both iNOS and AS after this treatment. As iNOS, AS, and AL were coinduced in rat tissues and cells, citrulline-arginine recycling seems to be important in NO synthesis under the conditions of stimulation.Nitric oxide (NO) is a major messenger molecule regulating blood vessel dilatation and immune function and functions as a neurotransmitter in the brain and peripheral nervous system (see Refs. 1-3 for reviews). NO is synthesized from arginine by nitric oxide synthase (NOS), 1 generating citrulline as another product. Cellular NO production is absolutely dependent on availability of arginine. This amino acid can be obtained from exogenous sources via the blood circulation, from intracellular protein degradation, or by endogenous synthesis of arginine.Major sites of arginine synthesis in ureotelic animals are the liver, where arginine generated in the urea cycle (ornithine cycle) is rapidly converted to urea and ornithine by arginase, and the kidney, where arginine is synthesized from citrulline and released into the blood circulation (see Ref. 4 for a review). However, other tissues and cell types also contain low levels of argininosuccinate synthetase (AS) and argininosuccinate lyase (AL), which together synthesize arginine from citrulline (5-8). Therefore, arginine can be generated from citrulline which is produced as a co-product of the NOS reaction, forming a cycle which could be termed the "citrulline-NO cycle" (9) or "arginine-citrulline cycle" (10). Vascular endothelial cells can convert citrulline to arginine (11), and this conversion is increased when cells are stimulated to produce NO (12). Cytokine-activated macrophages, which produ...

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Section: Discussionmentioning

confidence: 99%

Coinduction of Nitric Oxide Synthase, Argininosuccinate Synthetase, and Argininosuccinate Lyase in Lipopolysaccharide-treated Rats

Nagasaki

Gotoh

Takeya

et al. 1996

Journal of Biological Chemistry

121

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“…Human IFN-␣ and IFN-␤ were generous gifts from Dr. Duc-Goiran (INSERM, U361). The rabbit anti-liver NOS antibody (22) was a generous gift of Dr Ohshima (C.I.R.C., Lyon, France).…”

Section: Methodsmentioning

confidence: 99%

Inhibition of Inducible Nitric Oxide Synthase Expression by Interferons α and β in Bovine Retinal Pigmented Epithelial Cells

Faure

Courtois

Goureau

1997

Journal of Biological Chemistry

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“…20 After incubation periods with respective test compounds, VSMCs in culture were harvested and sonicated in ice-cold Tris buffer containing 50 mmol/L Tris-HCl (pH 7.5), 0.5 mmol/L EDTA, 0.5 mmol/L EGTA, 1 mmol/L leupeptin, 0.1 mmol/L phenylmethylsulfonyl fluoride, and 1 mmol/L dithiothreitol. The homogenate was centrifuged at 100 000g for 60 minutes at 4°C.…”

Section: Western Analysismentioning

confidence: 99%

Prostaglandin D ₂ Inhibits Inducible Nitric Oxide Synthase Expression in Rat Vascular Smooth Muscle Cells

Nagoshi

Uehara

Kanai

et al. 1998

Circulation Research

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Vascular smooth muscle cells (VSMCs) as well as macrophages have been shown to generate a substantial amount of NO in inflammatory vascular lesions. Prostaglandin (PG) D2 (PGD2) is produced by inflammatory cells, including mast cells and macrophages. We investigated whether PGD2 modulates NO metabolism in rat VSMCs. PGD2 at a concentration of 10(-7) mol/L or greater dose-dependently inhibited nitrite accumulation in the medium of cultured VSMCs stimulated with interleukin 1beta (IL-1beta). In a dose-response analysis of IL-1beta and nitrite accumulation, PGD2 was seen to decrease the maximal ability of VSMCs to generate NO, arguing against competition by PGD2 at cytokine receptors. Northern analysis showed that PGD2 suppresses induction of inducible NO synthase (iNOS) mRNA in IL-1beta-stimulated VSMCs, with consequent inhibition of iNOS protein expression in Western analysis. A thromboxane A2 (TXA2) analogue, U46619 (10(-5) mol/L), produced less inhibition of NO generation than did PGD2. Neither the PGI2 analog carbaprostacyclin nor PGE1 showed any inhibition. PGD2 dose-dependently inhibited NO generation despite the addition of the TXA2 antagonist SQ29548. PGJ2, delta12-PGJ2, and 15-deoxy-delta12,14-PGJ2, all metabolites of PGD2, were as potent as or slightly stronger than PGD2 in the inhibition of NO generation. These data suggest that PGD2 suppresses NO generation in VSMCs by inhibiting iNOS mRNA expression, most likely through the cascade of the PGJ2 series rather than through the TX receptor or cAMP upregulation. Such action makes it likely that PGD2 regulates NO metabolism in vascular lesions.

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Polyclonal antibody against an inducible form of nitric oxide synthase purified from the liver of rats treated with Propionibacterium acnes and lipopolysaccharide

Cited by 54 publications

References 9 publications

Coinduction of Nitric Oxide Synthase, Argininosuccinate Synthetase, and Argininosuccinate Lyase in Lipopolysaccharide-treated Rats

Coinduction of Nitric Oxide Synthase, Argininosuccinate Synthetase, and Argininosuccinate Lyase in Lipopolysaccharide-treated Rats

Inhibition of Inducible Nitric Oxide Synthase Expression by Interferons α and β in Bovine Retinal Pigmented Epithelial Cells

Prostaglandin D ₂ Inhibits Inducible Nitric Oxide Synthase Expression in Rat Vascular Smooth Muscle Cells

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Polyclonal antibody against an inducible form of nitric oxide synthase purified from the liver of rats treated with Propionibacterium acnes and lipopolysaccharide

Cited by 54 publications

References 9 publications

Coinduction of Nitric Oxide Synthase, Argininosuccinate Synthetase, and Argininosuccinate Lyase in Lipopolysaccharide-treated Rats

Coinduction of Nitric Oxide Synthase, Argininosuccinate Synthetase, and Argininosuccinate Lyase in Lipopolysaccharide-treated Rats

Inhibition of Inducible Nitric Oxide Synthase Expression by Interferons α and β in Bovine Retinal Pigmented Epithelial Cells

Prostaglandin D 2 Inhibits Inducible Nitric Oxide Synthase Expression in Rat Vascular Smooth Muscle Cells

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Prostaglandin D ₂ Inhibits Inducible Nitric Oxide Synthase Expression in Rat Vascular Smooth Muscle Cells