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
.jpg)
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/9048
Ver los metadatos del registro completo
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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 Técnicas2025-10-22T11:42:59Zoai: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:34982025-10-22 11:42:59.718CONICET 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 |
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info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
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article |
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publishedVersion |
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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 |
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eng |
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eng |
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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/ |
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openAccess |
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https://creativecommons.org/licenses/by/2.5/ar/ |
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application/pdf application/pdf |
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Public Library Of Science |
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Public Library Of Science |
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