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dc.contributor.author
Rigazio, Cristina Sandra
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dc.contributor.author
Hernandez, Matias
dc.contributor.author
Corral, Ricardo Santiago
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dc.date.available
2018-02-05T17:21:08Z
dc.date.issued
2014-06
dc.identifier.citation
Rigazio, Cristina Sandra; Hernandez, Matias; Corral, Ricardo Santiago; Cardiopathogenic mediators generated by GATA4 signaling upon co-activation with endothelin-1 and Trypanosoma cruzi infection; Academic Press Ltd-elsevier Science Ltd; Microbial Pathogenesis; 73; 6-2014; 47-52
dc.identifier.issn
0882-4010
dc.identifier.uri
http://hdl.handle.net/11336/35609
dc.description.abstract
Trypanosoma cruzi (Tc), the etiological agent of Chagas disease, triggers multiple responses in the myocardium, a central organ of infection and pathology in the host. Parasite-driven induction of diverse regulators of cardiovascular function, including the vasoconstrictor endothelin-1 (ET-1), the inducible form of nitric oxide synthase (iNOS) and the B-type natriuretic peptide (BNP), has been linked to the development of severe chagasic cardiomyopathy. Our current goal was to analyze the participation of the zinc finger transcription factor GATA4, critically implicated in pathological cardiac hypertrophic response, in the generation of key mediators involved in the pathogenesis of Tc-elicited heart dysfunction. In this study, we found that the combined effects of Tc and ET-1 on atrial myocytes promoted the protein expression, phosphorylation and DNA-binding activity of GATA4, leading to augmented protein levels of iNOS and increased nitric oxide release. Moreover, Tc- and ET-1-co-activation of cardiomyocytes resulted in enhanced GATA4-dependent secretion of BNP. Accordingly, mice with chronic chagasic cardiomyopathy showed increased expression of GATA4, iNOS and BNP at inflammatory lesions in cardiac muscle. Our findings support a role for the GATA4 signaling pathway in the myocardial production of pathogenic mediators associated with Chagas heart disease, and may help define novel therapeutic targets.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Academic Press Ltd-elsevier Science Ltd
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Chagas Cardiomyopathy
dc.subject
Trypanosoma Cruzi
dc.subject
Endothelin-1
dc.subject
Gata4
dc.subject.classification
Inmunología
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dc.subject.classification
Medicina Básica
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dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
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dc.title
Cardiopathogenic mediators generated by GATA4 signaling upon co-activation with endothelin-1 and Trypanosoma cruzi infection
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2018-02-05T13:38:14Z
dc.journal.volume
73
dc.journal.pagination
47-52
dc.journal.pais
Estados Unidos
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dc.journal.ciudad
Amsterdam
dc.description.fil
Fil: Rigazio, Cristina Sandra. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños "Ricardo Gutiérrez"; Argentina
dc.description.fil
Fil: Hernandez, Matias. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños "Ricardo Gutiérrez"; Argentina
dc.description.fil
Fil: Corral, Ricardo Santiago. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños "Ricardo Gutiérrez"; Argentina
dc.journal.title
Microbial Pathogenesis
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1016/j.micpath.2014.06.001
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0882401014000837
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