Title

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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