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

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 chag...

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Detalles Bibliográficos
Autores: Corral, Ricardo S, Guerrero, Néstor A, Cuervo, Henar, Gironès, Núria, Fresno, Manuel
Tipo de recurso: artículo
Fecha de publicación:2013
País:España
Institución:Instituto de Salud Carlos III (ISCIII)
Repositorio:Repisalud
Idioma:inglés
OAI Identifier:oai:repisalud.isciii.es:20.500.12105/17198
Acceso en línea:http://hdl.handle.net/20.500.12105/17198
Access Level:acceso abierto
Palabra clave:Animals
Atrial Natriuretic Factor
Calcineurin
Calcium
Cyclooxygenase 2
Endothelin-1
Gene Expression Profiling
Inflammation
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Monocytes
Myocytes, Cardiac
NFATC Transcription Factors
Natriuretic Peptide, C-Type
Protein Precursors
Signal Transduction
Thromboxane-A Synthase
Trypanosoma cruzi
Descripción
Sumario: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 Ca(2+)/calcineurin (Cn)/nuclear factor of activated T cells (NFAT) signaling pathway in atrial myocytes, leading to COX-2 protein expression and increased eicosanoid (prostaglandins E(2) and F(2α), thromboxane A(2)) 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 Ca(2+)/Cn/NFAT cascade in T. cruzi-mediated myocardial production of inflammatory mediators and may help define novel therapeutic targets.