Temporal patterns of tyrosine nitration in embryo heart development

Authors

    Authors

    L. Viera; M. Radmilovich; M. R. Vargas; C. N. Dennys; L. Wilson; S. Barnes; M. C. Franco; J. S. Beckman;A. G. Estevez

    Comments

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    Abbreviated Journal Title

    Free Radic. Biol. Med.

    Keywords

    Nitrotyrosine; Heart; Development; Nitric oxide synthase; Free radicals; NITRIC-OXIDE SYNTHASE; PEROXYNITRITE-INDUCED APOPTOSIS; CARBONATE; RADICAL-ANION; MICE LACKING; PC12 CELLS; SIGNALING PATHWAYS; REPERFUSION; INJURY; PROTEIN NITRATION; REACTIVE NITROGEN; STRESS; Biochemistry & Molecular Biology; Endocrinology & Metabolism

    Abstract

    Tyrosine nitration is a biomarker for the production of peroxynitrite and other reactive nitrogen species. Nitrotyrosine immunoreactivity is present in many pathological conditions including several cardiac diseases. Because the events observed during heart failure may recapitulate some aspects of development, we tested whether nitrotyrosine is present during normal development of the rat embryo heart and its potential relationship in cardiac remodeling through apoptosis. Nitric oxide production is highly dynamic during development, but whether peroxynitrite and nitrotyrosine are formed during normal embryonic development has received little attention. Rat embryo hearts exhibited strong nitrotyrosine immunoreactivity in endocardial and myocardial cells of the atria and ventricles from E12 to E18. After E18, nitrotyrosine staining faded and disappeared entirely by birth. Tyrosine nitration in the myocardial tissue coincided with elevated protein expression of nitric oxide synthases (eNOS and iNOS). The immunoreactivity for these NOS isoforms remained elevated even after nitrotyrosine had disappeared. Tyrosine nitration did not correlate with cell death or proliferation of cardiac cells. Analysis of tryptic peptides by MALDI-TOF showed that nitration occurs in actin, myosin, and the mitochondrial ATP synthase alpha chain. These results suggest that reactive nitrogen species are not restricted to pathological conditions but may play a role during normal embryonic development. (c) 2012 Elsevier Inc. All rights reserved.

    Journal Title

    Free Radical Biology and Medicine

    Volume

    55

    Publication Date

    1-1-2013

    Document Type

    Article

    Language

    English

    First Page

    101

    Last Page

    108

    WOS Identifier

    WOS:000315009600012

    ISSN

    0891-5849

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