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Blood, 15 July 2004, Vol. 104, No. 2, pp. 462-469. Prepublished online as a Blood First Edition Paper on March 25, 2004; DOI 10.1182/blood-2003-08-2990. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-08-2990v1 104/2/462    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Gilchrist, M. Articles by Befus, A. D. Search for Related Content PubMed PubMed Citation Articles by Gilchrist, M. Articles by Befus, A. D. Related Collections Signal Transduction Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Expression, localization, and regulation of NOS in human mast cell lines: effects on leukotriene production Mark Gilchrist, Scott D. McCauley, and A. Dean Befus From the Glaxo-Heritage Asthma Research Laboratory, Pulmonary Research Group, Department of Medicine, University of Alberta, Edmonton, AB, Canada. Nitric oxide (NO) is a potent radical produced by nitric oxide synthase (NOS) and has pleiotrophic activities in health and disease. As mast cells (MCs) play a central role in both homeostasis and pathology, we investigated NOS expression and NO production in human MC populations. Endothelial NOS (eNOS) was ubiquitously expressed in both human MC lines and skin-derived MCs, while neuronal NOS (nNOS) was variably expressed in the MC populations studied. The inducible (iNOS) isoform was not detected in human MCs. Both growth factor-independent (HMC-1) and -dependent (LAD 2) MC lines showed predominant nuclear eNOS protein localization, with weaker cytoplasmic expression. nNOS showed exclusive cytoplasmic localization in HMC-1. Activation with Ca2+ ionophore (A23187) or IgE-anti-IgE induced eNOS phosphorylation and translocation to the nucleus and nuclear and cytoplasmic NO formation. eNOS colocalizes with the leukotriene (LT)-initiating enzyme 5-lipoxygenase (5-LO) in the MC nucleus. The NO donor, S-nitrosoglutathione (SNOG), inhibited, whereas the NOS inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), potentiated LT release in a dose-dependent manner. Thus, human MC lines produce NO in both cytoplasmic and nuclear compartments, and endogenously produced NO can regulate LT production by MCs. (Blood. 2004;104: 462-469) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. Inoue, Y. Suzuki, T. Yoshimaru, and C. Ra Nitric oxide protects mast cells from activation-induced cell death: the role of the phosphatidylinositol-3 kinase-Akt-endothelial nitric oxide synthase pathway J. Leukoc. Biol., May 1, 2008; 83(5): 1218 - 1229. [Abstract] [Full Text] [PDF] M. Marcet-Palacios, M. Ulanova, F. Duta, L. Puttagunta, S. Munoz, D. Gibbings, M. Radomski, L. Cameron, I. Mayers, and A. D. Befus The Transcription Factor Wilms Tumor 1 Regulates Matrix Metalloproteinase-9 through a Nitric Oxide-Mediated Pathway J. Immunol., July 1, 2007; 179(1): 256 - 265. [Abstract] [Full Text] [PDF] R. F. Machado, A. Anthi, M. H. Steinberg, D. Bonds, V. Sachdev, G. J. Kato, A. M. Taveira-DaSilva, S. K. Ballas, W. Blackwelder, X. Xu, et al. N-terminal pro-brain natriuretic peptide levels and risk of death in sickle cell disease. JAMA, July 19, 2006; 296(3): 310 - 318. [Abstract] [Full Text] [PDF] F. Gobeil Jr., T. Zhu, S. Brault, A. 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