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Gene Review

NOS2  -  nitric oxide synthase 2, inducible

Gallus gallus

Synonyms: INOS, NOS2A
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Disease relevance of NOS2A

  • These findings document for the first time an iNOS whose mRNA levels are regulated by Ca2+ or PMA, but not inflammatory stimuli, and the autocrine production of NO as a Ca2+ sensing signal to suppress osteoclast bone resorption [1].
  • Clear induction of the gene was seen in splenocytes after exposure to Vibrio anguillarum in vivo, and after stimulation with LPS in vitro. iNOS message was first seen 2 h after stimulation, and was still apparent 24 h post-stimulation, the last timing studies [2].
  • Compared to GB2, macrophages from K-strain expressed higher iNOS mRNA as quantitated by reverse transcriptase polymerase (RT-PCR) chain reaction after stimulation with 1 microgram/ml of Escherichia coli (E. coli) lipopolysaccharide (LPS) [3].
  • Identification by electron microscopy of the maturation steps in vaccinia virus morphogenesis inhibited by the interferon-induced enzymes, protein kinase (PKR), 2-5A synthetase, and nitric oxide synthase (iNOS) [4].
  • 1. To clarify the effect of cold-induced pulmonary hypertension on endothelial and inducible nitric oxide synthase (eNOS and iNOS) mRNA expression in the lung of broiler chickens, semi quantitative reverse transcription-PCR was performed on total RNAs isolated from lungs of the broiler chickens exposed to 5 weeks of cold stress [5].

High impact information on NOS2A

  • Seven days later, when challenged with the very virulent RB-1B strain of MDV, the spleens of chickens treated with fp/cMGF showed increased expression of the inducible nitric oxide synthase (iNOS) gene compared to those of control chickens and fp/M3-treated chickens [6].
  • Treatment of CEF culture, prepared from 11-day-old embryos, with recombinant chicken gamma interferon (rChIFN-gamma) and lipopolysaccharide (LPS) resulted in production of NO which was suppressed by the addition of N(G)-monomethyl L-arginine (NMMA), an inhibitor of inducible NO synthase (iNOS) [7].
  • Moreover, in the chicken macrophage cell line HD-11, CC chemokines, MGF, IL-1beta, and iNOS were inducible by IFN-gamma, suggesting that macrophages may be one of the cell populations involved in the upregulation of these cytokines observed in vivo during infection with Eimeria [8].
  • RNase protection assay also showed that lipopolysaccharide provoked 14.6 +/- 5.1-fold increases (n = 6, p < 0.05) in the iNOS mRNA signals within 6 h [9].
  • Northern blot analysis revealed that chicken iNOS mRNA of approximately 4.5 kb was induced by lipopolysaccharide within 6 h in the cultured myocytes [9].

Chemical compound and disease context of NOS2A

  • In searching for potential modulators of osteoclast iNOS, protein kinase C activation [by phorbol 12-myristate 13-acetate (PMA)] and intracellular Ca2+ rises (A23187) were each found to elevate osteoclast iNOS mRNA and protein levels, while increasing NO release and reducing osteoclast bone resorption [1].

Biological context of NOS2A

  • CONCLUSION: As like as the nucleotide and amino acid sequences, the myocardial effects of the iNOS may also be evolutionary conserved [9].
  • In addition, nuclear extracts obtained from myoblasts that were competent for fusion, but not those from proliferating cells or from fully differentiated myotubes, were capable of binding to the consensus NF-kappaB site in the promoter region of the gene encoding iNOS [10].
  • In addition, a partial cDNA sequence of NOS obtained by reverse transcription PCR on total RNA from chick myoblasts was found to be identical with that of the inducible type of NOS (iNOS) from chick macrophage [10].
  • GW9662, a PPARgamma antagonist, prevented (P < 0.01) the lutein-induced iNOS mRNA downregulation in HD11 cells [11].
  • Our findings have identified the steps in VV morphogenesis inhibited by PKR, 2-5A, and iNOS, provided a distinction between these effects, and highlighted a functional redundancy of the IFN system to block viral infection and to induce apoptosis [4].

Anatomical context of NOS2A

  • RT-PCR analysis demonstrated that LPS, LTA, and CpG-ODN induced inducible nitric oxide synthase (iNOS) expression in monocytes; whereas the other agonists did not [12].
  • Avian osteoclasts expressed both iNOS messenger RNA (mRNA) and protein [1].
  • We have recently reported that 1,25-(OH)2D synthesis in the chick myelomonocytic cell line HD-11 is restricted by inhibition of iNOS [13].
  • Thus chick myoblast NOS must belong to the family of iNOS [10].
  • In order to elucidate further the role of nitric oxide (NO) as an endogenous antiangiogenic mediator, mRNA expression of inducible nitric oxide synthase (iNOS), enzyme activity and production of NO were determined in the chick chorioallantoic membrane (CAM), an in vivo model of angiogenesis [14].

Associations of NOS2A with chemical compounds

  • The iNOS activity (+300%, P < 0.05) as well as the intracellular cGMP contents (+75%, P < 0.01) were significantly augmented in the lipopolysaccharide-stimulated cells [9].
  • The iNOS activity was estimated from conversion rates of L-arginine to L-citrulline and intracellular cGMP contents were measured with radioimmunoassay [9].
  • The iNOS selective inhibitor aminoguanidine suppressed stimulated osteoclast NO production elicited by either signal, but reversed only the resorption inhibition due to raised Ca2+ [1].
  • Cells of the monocyte/macrophage lineage are capable of both nitric oxide (NO) and 1,25-dihydroxyvitamin D [1, 25-(OH)2D] production through expression of inducible nitric oxide synthase (iNOS) and a putative 25-hydroxyvitamin D (25-OHD)-1-hydroxylase, respectively [13].
  • At 3% dietary fat or up to 15 micromol/L EPA in the medium, increasing lutein increased the iNOS mRNA [11].

Other interactions of NOS2A

  • However, there was no difference between these two groups of birds in the expression of interferon (IFN)-gamma, IL-4, IL-12 and inducible nitric oxide synthase (iNOS) genes on day 21 post-infection [15].

Analytical, diagnostic and therapeutic context of NOS2A

  • METHODS: An iNOS cDNA clone was isolated by RT-PCR from the 10-day old cultured chick embryonic ventricular myocytes stimulated with 10 micrograms/ml of lipopolysaccharide [9].
  • 5. Comparing the treatment group with its control group, iNOS mRNA level was significantly higher at 21 d of age in the cold-exposed chickens [5].
  • However, vaccination with HVT 3 days before RB-1B inoculation restored strong iNOS gene expression in the spleen 1 week later and inducible NO production 3 weeks later [16].


  1. Ca2+ or phorbol ester but not inflammatory stimuli elevate inducible nitric oxide synthase messenger ribonucleic acid and nitric oxide (NO) release in avian osteoclasts: autocrine NO mediates Ca2+-inhibited bone resorption. Sunyer, T., Rothe, L., Kirsch, D., Jiang, X., Anderson, F., Osdoby, P., Collin-Osdoby, P. Endocrinology (1997) [Pubmed]
  2. Cloning of iNOS in the small spotted catshark (Scyliorhinus canicula). Reddick, J.I., Goostrey, A., Secombes, C.J. Dev. Comp. Immunol. (2006) [Pubmed]
  3. Interleukin-1beta does not contribute to genetic strain-based differences in iNOS expression and activity in chicken macrophages. Dil, N., Qureshi, M.A. Dev. Comp. Immunol. (2003) [Pubmed]
  4. Identification by electron microscopy of the maturation steps in vaccinia virus morphogenesis inhibited by the interferon-induced enzymes, protein kinase (PKR), 2-5A synthetase, and nitric oxide synthase (iNOS). Esteban, M., Patiño, C. J. Interferon Cytokine Res. (2000) [Pubmed]
  5. Evaluation of endothelial and inducible nitric oxide synthase mRNA expression in the lung of broiler chickens with developmental pulmonary hypertension due to cold stress. Teshfam, M., Brujeni, G.N., Hassanpour, H. Br. Poult. Sci. (2006) [Pubmed]
  6. Protective effect of avian myelomonocytic growth factor in infection with Marek's disease virus. Djeraba, A., Musset, E., Lowenthal, J.W., Boyle, D.B., Chaussé, A.M., Péloille, M., Quéré, P. J. Virol. (2002) [Pubmed]
  7. Inhibitory effects of nitric oxide and gamma interferon on in vitro and in vivo replication of Marek's disease virus. Xing, Z., Schat, K.A. J. Virol. (2000) [Pubmed]
  8. Analysis of chicken mucosal immune response to Eimeria tenella and Eimeria maxima infection by quantitative reverse transcription-PCR. Laurent, F., Mancassola, R., Lacroix, S., Menezes, R., Naciri, M. Infect. Immun. (2001) [Pubmed]
  9. Molecular cloning and expression of inducible nitric oxide synthase in chick embryonic ventricular myocytes. Shimizu, T., Kinugawa, K., Sugishita, Y., Sugishita, K., Harada, K., Matsui, H., Kohmoto, O., Serizawa, T., Takahashi, T. Cardiovasc. Res. (1998) [Pubmed]
  10. NF-kappaB-dependent expression of nitric oxide synthase is required for membrane fusion of chick embryonic myoblasts. Lee, K.H., Kim, D.G., Shin, N.Y., Song, W.K., Kwon, H., Chung, C.H., Kang, M.S. Biochem. J. (1997) [Pubmed]
  11. Lutein and eicosapentaenoic acid interact to modify iNOS mRNA levels through the PPARgamma/RXR pathway in chickens and HD11 cell lines. Selvaraj, R.K., Klasing, K.C. J. Nutr. (2006) [Pubmed]
  12. Profile of Toll-like receptor expressions and induction of nitric oxide synthesis by Toll-like receptor agonists in chicken monocytes. He, H., Genovese, K.J., Nisbet, D.J., Kogut, M.H. Mol. Immunol. (2006) [Pubmed]
  13. Coordinate regulation of nitric oxide and 1,25-dihydroxyvitamin D production in the avian myelomonocytic cell line HD-11. Adams, J.S., Ren, S.Y., Arbelle, J.E., Shany, S., Gacad, M.A. Endocrinology (1995) [Pubmed]
  14. Nitric oxide synthase expression, enzyme activity and NO production during angiogenesis in the chick chorioallantoic membrane. Pipili-Synetos, E., Kritikou, S., Papadimitriou, E., Athanassiadou, A., Flordellis, C., Maragoudakis, M.E. Br. J. Pharmacol. (2000) [Pubmed]
  15. Cytokine gene expression patterns associated with immunization against Marek's disease in chickens. Abdul-Careem, M.F., Hunter, B.D., Parvizi, P., Haghighi, H.R., Thanthrige-Don, N., Sharif, S. Vaccine (2007) [Pubmed]
  16. Similar pattern of iNOS expression, NO production and cytokine response in genetic and vaccination-acquired resistance to Marek's disease. Djeraba, A., Musset, E., Bernardet, N., Le Vern, Y., Quéré, P. Vet. Immunol. Immunopathol. (2002) [Pubmed]
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