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• W1566961983 abstract "HomeCirculationVol. 103, No. 14Cross-Talk Between Constitutive and Inducible Nitric Oxide Synthases Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBCross-Talk Between Constitutive and Inducible Nitric Oxide Synthases Hisanori Suzuki Marco Colasanti Hisanori SuzukiHisanori Suzuki Department of Neurological Science and Vision, University of Verona, Verona, Italy Search for more papers by this author Marco ColasantiMarco Colasanti Department of Biology, University of Roma 3, Roma, Italy Search for more papers by this author Originally published10 Apr 2001https://doi.org/10.1161/01.CIR.103.14.e81Circulation. 2001;103:e81To the Editor,We read with great interest the recent work by Kanno et al1 describing the protective effect of nitric oxide (NO) against myocardial ischemia/reperfusion injury and were struck by the other phenomenon associated with it: superinduction of inducible NO synthase (iNOS) in endothelial NO synthase (eNOS) knockout mice. Although the exact mechanism is unknown and apparently “paradoxical,” the absence of constitutive NO seems to increase inducible NO production. In this respect, the authors argued that the effect could be due to redox stress associated with the absence of NO.Recently, we published an article2 suggesting cross-talk between constitutive and inducible NOS using NO as a modulator. In particular, low (ie, physiological) NO levels inhibit iNOS transcription by inactivating nuclear factor-κB (NF-κB).345 However, when NO levels decrease beneath a putative threshold value (eg, as in eNOS knockout cardiomyocytes), they may not be sufficient to keep NF-κB suppressed, thus creating the favorable conditions for superinduction of NOS-II expression. Interestingly, the adaptive mechanism that the authors propose may simply reflect an acquired activation of NF-κB due to the absence of NO, leading to the change in redox stress.Therefore, the work by Kanno et al1 introduces, for the first time, an ex vivo model indicating that intracellular amounts of NO may play a key role in modulating iNOS expression, thus providing further evidence for our hypothesis. However, other ex vivo or in vivo models should be examined to obtain more insight regarding the strict cross-talk between NO and NO synthases.Moreover, on the basis of evidence suggesting a beneficial effect of iNOS-produced NO,1 very low amounts of NO, which could potentially be harmful to the body by facilitating the induction of iNOS expression, may not (for the same reason) always be detrimental. The work by Kanno et al1 pointed out the importance of the physiologically present NO in downregulating the induction of iNOS. Attention should be paid to any trial that modulates intracellular amounts of NO. Any compound down-modulating the catalytic activity of constitutive NOS, such as specific inhibitors of constitutive NOS or NO donors that moderately increase intracellular NO levels, may exert more profound effects on the induction of iNOS expression than normally expected. References 1 Kanno S, Lee PC, Zhang Y, et al. Attenuation of myocardial ischemia/reperfusion injury by superinduction of inducible nitric oxide synthase. Circulation.2000; 101:2742–2748.CrossrefMedlineGoogle Scholar2 Colasanti M, Suzuki H. The dual personality of NO. Trends Pharmacol Sci.2000; 21:249-e252.CrossrefMedlineGoogle Scholar3 Colasanti M, Persichini T, Menegazzi M, et al. Induction of nitric oxide synthase mRNA expression: suppression by exogenous nitric oxide. J Biol Chem.1995; 270:26731–26733.CrossrefMedlineGoogle Scholar4 Colasanti M, Persichini T, Cavalieri E, et al. Rapid inactivation of NOS-I by lipopolysaccharide plus interferon-gamma–induced tyrosine phosphorylation. J Biol Chem.1999; 274:9915–9917.CrossrefMedlineGoogle Scholar5 Mariotto S, Cuzzolin L, Adami A, et al. Inhibition by sodium nitroprusside of the expression of inducible nitric oxide synthase in rat neutrophils. Br J Pharmacol.1995; 114:1105–1106.CrossrefMedlineGoogle ScholarcirculationahaCirculationCirculationCirculation0009-73221524-4539Lippincott Williams & WilkinsResponseKanno Shinichi, MD, PhD, Zhang Yuqing, MD, PhD, Ho Chien, PhD, Lee Paul C., MD, Griffith Bartley P., MD, Shears Larry L., MD, and Billiar Timothy R., MD10042001We are grateful to Dr Marco Colasanti and Prof Hisanori Suzuki for their comments and are pleased that they found our article of interest. They suggest a possible mechanism relating to our finding of superinduction of inducible nitric oxide synthase (iNOS) in the isolated hearts from endothelial NOS (eNOS) knockout mice subjected to warm ischemia reperfusion.Recently Dr Marco Colasanti and Prof Hisanori Suzuki published a review in Trends in Pharmacological ScienceR1 that presents a plausible mechanism for the superinduction of iNOS observed in our experiment. According to their review and previous work,R1R2R3R4 this paradoxical induction of iNOS can possibly be explained by the following hypothesis. Low concentrations of NO, maintained by the activity of constitutive NOS, suppress the activation of nuclear factor kB (NF-kB) under resting conditions. Therefore, it is reasonable to speculate that conditions that lead to a reduction in NO availability, such as suppressed or absent eNOS activity or removal of NO by other molecules (eg, oxygen radicals and heme-containing proteins), will facilitate NF-kB activation. Because NF-kB is one of the transcription factors required for the activation of the iNOS gene, this could contribute to the hyperinduction of iNOS. However, it is unlikely that this hypothesis alone explains the hyperinduction of iNOS. For instance, it does not explain the triggering mechanism for the activation of NF-kB and iNOS expression. This is most likely due to the increased production of oxygen radicals. Because NO can neutralize oxygen radicals, it is also possible that basal levels of NO have an antioxidant function and that the increased oxidative stress resulting from the absence of constitutive levels of NO contributes to the hyperinduction of iNOS at reperfusion. There is ample evidence that supplementation with low levels of NO donors or providing arginine can be protective in models of ischemia-reperfusion.Finally, we thank Dr Marco Colasanti and Prof Hisanori Suzuki for kindly suggesting a possible mechanism of superinduction of iNOS observed in eNOS knockout mice. Previous Back to top Next FiguresReferencesRelatedDetailsCited By Loeb E, El Asmar K, Trabado S, Gressier F, Colle R, Rigal A, Martin S, Verstuyft C, Fève B, Chanson P, Becquemont L and Corruble E (2020) Nitric Oxide Synthase activity in major depressive episodes before and after antidepressant treatment: Results of a large case-control treatment study, Psychological Medicine, 10.1017/S0033291720001749, 52:1, (80-89), Online publication date: 1-Jan-2022. González-Montero J, Brito R, Gajardo A and Rodrigo R (2018) Myocardial reperfusion injury and oxidative stress: Therapeutic opportunities, World Journal of Cardiology, 10.4330/wjc.v10.i9.74, 10:9, (74-86), Online publication date: 30-Sep-2018. Ben Chaaben A, Mariaselvam C, Salah S, Busson M, Dulphy N, Douik H, Ghanem A, Boukaouci W, Al Daccak R, Mamoghli T, Harzallah L, Bouassida J, Fortier C, Gritli S, Hamida J, Charron D, Krishnamoorthy R, Guemira F and Tamouza R (2015) Polymorphisms in oxidative stress-related genes are associated with nasopharyngeal carcinoma susceptibility, Immunobiology, 10.1016/j.imbio.2014.09.021, 220:1, (20-25), Online publication date: 1-Jan-2015. Hu C, Chen J, Dandapat A, Fujita Y, Inoue N, Kawase Y, Jishage K, Suzuki H, Li D, Hermonat P, Sawamura T and Mehta J (2008) LOX-1 abrogation reduces myocardial ischemia–reperfusion injury in mice, Journal of Molecular and Cellular Cardiology, 10.1016/j.yjmcc.2007.10.009, 44:1, (76-83), Online publication date: 1-Jan-2008. Djidjik R, Ghaffor M, Brun M, Gharnaout M, Salah S, Boukouaci W, Djidjik H, Benyounes A, Koumaravelou K, Krishnamoorthy R, Abbadi M, Charron D and Tamouza R (2007) Constitutive nitric oxide synthase gene polymorphisms and house dust mite respiratory allergy in an Algerian patient group, Tissue Antigens, 10.1111/j.1399-0039.2007.00976.x, 71:2, (160-164) Conti A, Miscusi M, Cardali S, Germanò A, Suzuki H, Cuzzocrea S and Tomasello F (2007) Nitric oxide in the injured spinal cord: Synthases cross-talk, oxidative stress and inflammation, Brain Research Reviews, 10.1016/j.brainresrev.2007.01.013, 54:1, (205-218), Online publication date: 1-Apr-2007. Ziaja M, Pyka J, Machowska A, Maslanka A and Plonka P (2007) Nitric Oxide Spin-Trapping and NADPH-Diaphorase Activity in Mature Rat Brain after Injury, Journal of Neurotrauma, 10.1089/neu.2007.0303, 24:12, (1845-1854), Online publication date: 1-Dec-2007. Sowden H, Naseem K and Tobin D (2005) Differential expression of nitric oxide synthases in human scalp epidermal and hair follicle pigmentary units: implications for regulation of melanogenesis, British Journal of Dermatology, 10.1111/j.1365-2133.2005.06718.x, 153:2, (301-309), Online publication date: 1-Aug-2005. Palomba L, Persichini T, Mazzone V, Colasanti M and Cantoni O (2004) Inhibition of Nitric-oxide Synthase-I (NOS-I)-dependent Nitric Oxide Production by Lipopolysaccharide plus Interferon-γ Is Mediated by Arachidonic Acid, Journal of Biological Chemistry, 10.1074/jbc.M312768200, 279:29, (29895-29901), Online publication date: 1-Jul-2004. Maggio D, Singh A, Iorgulescu J, Bleicher D, Ghosh M, Lopez M, Tuesta L, Flora G, Dietrich W and Pearse D (2017) Identifying the Long-Term Role of Inducible Nitric Oxide Synthase after Contusive Spinal Cord Injury Using a Transgenic Mouse Model, International Journal of Molecular Sciences, 10.3390/ijms18020245, 18:2, (245) April 10, 2001Vol 103, Issue 14 Advertisement Article InformationMetrics Copyright © 2001 by American Heart Associationhttps://doi.org/10.1161/01.CIR.103.14.e81 Originally publishedApril 10, 2001 PDF download Advertisement" @default.
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