Trypanosoma cruzi infection and endothelin-1 cooperatively activate pathogenic inflammatory pathways in cardiomyocytes

Autores
Corral, Ricardo Santiago; Guerrero, Néstor A.; Cuervo, Henar; Gironès, Núria; Fresno, Manuel
Año de publicación
2013
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Trypanosoma cruzi, the causative agent of Chagas disease, induces multiple responses in the heart, a critical organ of infection and pathology in the host. Among diverse factors, eicosanoids and the vasoactive peptide endothelin-1 (ET-1) have been implicated in the pathogenesis of chronic chagasic cardiomyopathy. In the present study, we found that T. cruzi infection in mice induces myocardial gene expression of cyclooxygenase-2 (Cox2) and thromboxane synthase (Tbxas1) as well as endothelin-1 (Edn1) and atrial natriuretic peptide (Nppa). T. cruzi infection and ET-1 cooperatively activated the calcium/calcineurin (Cn)/nuclear factor of activated T cells (NFAT) signaling pathway in atrial myocytes, leading to COX-2 protein expression and increased eicosanoid (prostaglandins E2 and F2 alpha, thromboxane A2) release. Moreover, T. cruzi infection of ET-1-stimulated cardiomyocytes resulted in significantly enhanced production of atrial natriuretic peptide (ANP), a prognostic marker for impairment in cardiac function of chagasic patients. Our findings support an important role for the calcium/Cn/NFAT cascade in T. cruzi-mediated myocardial production of inflammatory mediators and may help define novel therapeutic targets.
Fil: Corral, Ricardo Santiago. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños "Ricardo Gutierrez"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Guerrero, Néstor A.. Consejo Superior de Investigaciones Cientificas; España. Universidad Autonoma de Madrid. Hospital Universitario de la Princesa; España
Fil: Cuervo, Henar. Consejo Superior de Investigaciones Cientificas; España
Fil: Gironès, Núria. Consejo Superior de Investigaciones Cientificas; España. Universidad Autonoma de Madrid. Hospital Universitario de la Princesa; España
Fil: Fresno, Manuel. Consejo Superior de Investigaciones Cientificas; España. Universidad Autonoma de Madrid. Hospital Universitario de la Princesa; España
Materia
TRYPANOSOMA CRUZI
ENDOTHELIN-1
CARDIOMYOCYTE
INFLAMMATION
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/9048

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spelling Trypanosoma cruzi infection and endothelin-1 cooperatively activate pathogenic inflammatory pathways in cardiomyocytesCorral, Ricardo SantiagoGuerrero, Néstor A.Cuervo, HenarGironès, NúriaFresno, ManuelTRYPANOSOMA CRUZIENDOTHELIN-1CARDIOMYOCYTEINFLAMMATIONhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Trypanosoma cruzi, the causative agent of Chagas disease, induces multiple responses in the heart, a critical organ of infection and pathology in the host. Among diverse factors, eicosanoids and the vasoactive peptide endothelin-1 (ET-1) have been implicated in the pathogenesis of chronic chagasic cardiomyopathy. In the present study, we found that T. cruzi infection in mice induces myocardial gene expression of cyclooxygenase-2 (Cox2) and thromboxane synthase (Tbxas1) as well as endothelin-1 (Edn1) and atrial natriuretic peptide (Nppa). T. cruzi infection and ET-1 cooperatively activated the calcium/calcineurin (Cn)/nuclear factor of activated T cells (NFAT) signaling pathway in atrial myocytes, leading to COX-2 protein expression and increased eicosanoid (prostaglandins E2 and F2 alpha, thromboxane A2) release. Moreover, T. cruzi infection of ET-1-stimulated cardiomyocytes resulted in significantly enhanced production of atrial natriuretic peptide (ANP), a prognostic marker for impairment in cardiac function of chagasic patients. Our findings support an important role for the calcium/Cn/NFAT cascade in T. cruzi-mediated myocardial production of inflammatory mediators and may help define novel therapeutic targets.Fil: Corral, Ricardo Santiago. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños "Ricardo Gutierrez"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Guerrero, Néstor A.. Consejo Superior de Investigaciones Cientificas; España. Universidad Autonoma de Madrid. Hospital Universitario de la Princesa; EspañaFil: Cuervo, Henar. Consejo Superior de Investigaciones Cientificas; EspañaFil: Gironès, Núria. Consejo Superior de Investigaciones Cientificas; España. Universidad Autonoma de Madrid. Hospital Universitario de la Princesa; EspañaFil: Fresno, Manuel. Consejo Superior de Investigaciones Cientificas; España. Universidad Autonoma de Madrid. Hospital Universitario de la Princesa; EspañaPublic Library Of Science2013-02info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/9048Corral, Ricardo Santiago; Guerrero, Néstor A.; Cuervo, Henar; Gironès, Núria; Fresno, Manuel; Trypanosoma cruzi infection and endothelin-1 cooperatively activate pathogenic inflammatory pathways in cardiomyocytes; Public Library Of Science; Neglected Tropical Diseases; 7; 2; 2-2013; 1-121935-2735enginfo:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pntd.0002034info:eu-repo/semantics/altIdentifier/url/http://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0002034info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3566987/info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:13:05Zoai:ri.conicet.gov.ar:11336/9048instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 10:13:06.224CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Trypanosoma cruzi infection and endothelin-1 cooperatively activate pathogenic inflammatory pathways in cardiomyocytes
title Trypanosoma cruzi infection and endothelin-1 cooperatively activate pathogenic inflammatory pathways in cardiomyocytes
spellingShingle Trypanosoma cruzi infection and endothelin-1 cooperatively activate pathogenic inflammatory pathways in cardiomyocytes
Corral, Ricardo Santiago
TRYPANOSOMA CRUZI
ENDOTHELIN-1
CARDIOMYOCYTE
INFLAMMATION
title_short Trypanosoma cruzi infection and endothelin-1 cooperatively activate pathogenic inflammatory pathways in cardiomyocytes
title_full Trypanosoma cruzi infection and endothelin-1 cooperatively activate pathogenic inflammatory pathways in cardiomyocytes
title_fullStr Trypanosoma cruzi infection and endothelin-1 cooperatively activate pathogenic inflammatory pathways in cardiomyocytes
title_full_unstemmed Trypanosoma cruzi infection and endothelin-1 cooperatively activate pathogenic inflammatory pathways in cardiomyocytes
title_sort Trypanosoma cruzi infection and endothelin-1 cooperatively activate pathogenic inflammatory pathways in cardiomyocytes
dc.creator.none.fl_str_mv Corral, Ricardo Santiago
Guerrero, Néstor A.
Cuervo, Henar
Gironès, Núria
Fresno, Manuel
author Corral, Ricardo Santiago
author_facet Corral, Ricardo Santiago
Guerrero, Néstor A.
Cuervo, Henar
Gironès, Núria
Fresno, Manuel
author_role author
author2 Guerrero, Néstor A.
Cuervo, Henar
Gironès, Núria
Fresno, Manuel
author2_role author
author
author
author
dc.subject.none.fl_str_mv TRYPANOSOMA CRUZI
ENDOTHELIN-1
CARDIOMYOCYTE
INFLAMMATION
topic TRYPANOSOMA CRUZI
ENDOTHELIN-1
CARDIOMYOCYTE
INFLAMMATION
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Trypanosoma cruzi, the causative agent of Chagas disease, induces multiple responses in the heart, a critical organ of infection and pathology in the host. Among diverse factors, eicosanoids and the vasoactive peptide endothelin-1 (ET-1) have been implicated in the pathogenesis of chronic chagasic cardiomyopathy. In the present study, we found that T. cruzi infection in mice induces myocardial gene expression of cyclooxygenase-2 (Cox2) and thromboxane synthase (Tbxas1) as well as endothelin-1 (Edn1) and atrial natriuretic peptide (Nppa). T. cruzi infection and ET-1 cooperatively activated the calcium/calcineurin (Cn)/nuclear factor of activated T cells (NFAT) signaling pathway in atrial myocytes, leading to COX-2 protein expression and increased eicosanoid (prostaglandins E2 and F2 alpha, thromboxane A2) release. Moreover, T. cruzi infection of ET-1-stimulated cardiomyocytes resulted in significantly enhanced production of atrial natriuretic peptide (ANP), a prognostic marker for impairment in cardiac function of chagasic patients. Our findings support an important role for the calcium/Cn/NFAT cascade in T. cruzi-mediated myocardial production of inflammatory mediators and may help define novel therapeutic targets.
Fil: Corral, Ricardo Santiago. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños "Ricardo Gutierrez"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Guerrero, Néstor A.. Consejo Superior de Investigaciones Cientificas; España. Universidad Autonoma de Madrid. Hospital Universitario de la Princesa; España
Fil: Cuervo, Henar. Consejo Superior de Investigaciones Cientificas; España
Fil: Gironès, Núria. Consejo Superior de Investigaciones Cientificas; España. Universidad Autonoma de Madrid. Hospital Universitario de la Princesa; España
Fil: Fresno, Manuel. Consejo Superior de Investigaciones Cientificas; España. Universidad Autonoma de Madrid. Hospital Universitario de la Princesa; España
description Trypanosoma cruzi, the causative agent of Chagas disease, induces multiple responses in the heart, a critical organ of infection and pathology in the host. Among diverse factors, eicosanoids and the vasoactive peptide endothelin-1 (ET-1) have been implicated in the pathogenesis of chronic chagasic cardiomyopathy. In the present study, we found that T. cruzi infection in mice induces myocardial gene expression of cyclooxygenase-2 (Cox2) and thromboxane synthase (Tbxas1) as well as endothelin-1 (Edn1) and atrial natriuretic peptide (Nppa). T. cruzi infection and ET-1 cooperatively activated the calcium/calcineurin (Cn)/nuclear factor of activated T cells (NFAT) signaling pathway in atrial myocytes, leading to COX-2 protein expression and increased eicosanoid (prostaglandins E2 and F2 alpha, thromboxane A2) release. Moreover, T. cruzi infection of ET-1-stimulated cardiomyocytes resulted in significantly enhanced production of atrial natriuretic peptide (ANP), a prognostic marker for impairment in cardiac function of chagasic patients. Our findings support an important role for the calcium/Cn/NFAT cascade in T. cruzi-mediated myocardial production of inflammatory mediators and may help define novel therapeutic targets.
publishDate 2013
dc.date.none.fl_str_mv 2013-02
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/9048
Corral, Ricardo Santiago; Guerrero, Néstor A.; Cuervo, Henar; Gironès, Núria; Fresno, Manuel; Trypanosoma cruzi infection and endothelin-1 cooperatively activate pathogenic inflammatory pathways in cardiomyocytes; Public Library Of Science; Neglected Tropical Diseases; 7; 2; 2-2013; 1-12
1935-2735
url http://hdl.handle.net/11336/9048
identifier_str_mv Corral, Ricardo Santiago; Guerrero, Néstor A.; Cuervo, Henar; Gironès, Núria; Fresno, Manuel; Trypanosoma cruzi infection and endothelin-1 cooperatively activate pathogenic inflammatory pathways in cardiomyocytes; Public Library Of Science; Neglected Tropical Diseases; 7; 2; 2-2013; 1-12
1935-2735
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pntd.0002034
info:eu-repo/semantics/altIdentifier/url/http://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0002034
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3566987/
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Public Library Of Science
publisher.none.fl_str_mv Public Library Of Science
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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