Use este identificador para citar ou linkar para este item:
https://www.arca.fiocruz.br/handle/icict/36714
Tipo de documento
ArtigoDireito Autoral
Acesso aberto
Data de embargo
2020-04-25
Coleções
- INI - Artigos de Periódicos [3488]
Metadata
Mostrar registro completo
DYNAMIC DENITROSYLATION VIA S-NITROSOGLUTATHIONE REDUCTASE REGULATES CARDIOVASCULAR FUNCTION
Autor(es)
Afiliação
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA.
Case Western Reserve University. Institute for Transformative Molecular Medicine. Department of Medicine. Cleveland, OH, USA / University Hospitals. Cleveland, OH, USA.
Duke University. Department of Medicine. Durham, NC, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA / Miami Veterans Affairs Healthcare System. Nephrology-Hypertension Section. Miami, FL, USA.
Case Western Reserve University. Institute for Transformative Molecular Medicine. Department of Medicine. Cleveland, OH, USA / University Hospitals. Cleveland, OH, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA.
Case Western Reserve University. Institute for Transformative Molecular Medicine. Department of Medicine. Cleveland, OH, USA / University Hospitals. Cleveland, OH, USA.
Duke University. Department of Medicine. Durham, NC, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA / Miami Veterans Affairs Healthcare System. Nephrology-Hypertension Section. Miami, FL, USA.
Case Western Reserve University. Institute for Transformative Molecular Medicine. Department of Medicine. Cleveland, OH, USA / University Hospitals. Cleveland, OH, USA.
University of Miami Miller School of Medicine. Interdisciplinary Stem Cell Institute. Miami, FL, USA.
Resumo em Inglês
Although protein S-nitrosylation is increasingly recognized as mediating nitric oxide (NO) signaling, roles for protein denitrosylation in physiology remain unknown. Here, we show that S-nitrosoglutathione reductase (GSNOR), an enzyme that governs levels of S-nitrosylation by promoting protein denitrosylation, regulates both peripheral vascular tone and β-adrenergic agonist-stimulated cardiac contractility, previously ascribed exclusively to NO/cGMP. GSNOR-deficient mice exhibited reduced peripheral vascular tone and depressed β-adrenergic inotropic responses that were associated with impaired β-agonist–induced denitrosylation of cardiac
ryanodine receptor 2 (RyR2), resulting in calcium leak. These results indicate that systemic hemodynamic responses (vascular tone and cardiac contractility), both under basal conditions and after adrenergic activation, are regulated through concerted actions of NO synthase/GSNOR and that aberrant denitrosylation impairs cardiovascular function. Our findings support the notion that dynamic S-nitrosylation/denitrosylation reactions are essential in cardiovascular regulation.
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