Endogenous osteopontin induces myocardial CCL5 and MMP-2 activation that contributes to inflammation and cardiac remodeling in a mouse model of chronic Chagas heart disease

Cardiac dysfunction with progressive inflammation and fibrosis is a hallmark of Chagas disease caused by persistent Trypanosoma cruzi infection. Osteopontin (OPN) is a pro-inflammatory cytokine that orchestrates mechanisms controlling cell recruitment and cardiac architecture. Our main goal was to s...

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Veröffentlicht in:	Biochimica et biophysica acta. Molecular basis of disease 2018-01, Vol.1864 (1), p.11-23
Hauptverfasser:	Caballero, Eugenia Pérez, Santamaría, Miguel H., Corral, Ricardo S.
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Atrial Remodeling - genetics Atrial Remodeling - immunology Cardiac remodeling Cells, Cultured Chagas cardiomyopathy Chagas Cardiomyopathy - genetics Chagas Cardiomyopathy - immunology Chagas Cardiomyopathy - metabolism Chagas Cardiomyopathy - pathology Chemokine CCL5 - metabolism Disease Models, Animal Endomyocardial Fibrosis - genetics Endomyocardial Fibrosis - metabolism Endomyocardial Fibrosis - pathology Inflammation Inflammation - genetics Inflammation - metabolism Inflammation - pathology Male Matrix Metalloproteinase 2 - metabolism Mice Mice, Inbred C3H Mice, Inbred C57BL Mice, Knockout Myocarditis - genetics Myocarditis - immunology Myocarditis - metabolism Myocarditis - pathology Myocardium - immunology Myocardium - metabolism Myocardium - pathology Osteopontin Osteopontin - genetics Osteopontin - physiology Trypanosoma cruzi Ventricular Remodeling - genetics Ventricular Remodeling - immunology
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Zusammenfassung:	Cardiac dysfunction with progressive inflammation and fibrosis is a hallmark of Chagas disease caused by persistent Trypanosoma cruzi infection. Osteopontin (OPN) is a pro-inflammatory cytokine that orchestrates mechanisms controlling cell recruitment and cardiac architecture. Our main goal was to study the role of endogenous OPN as a modulator of myocardial CCL5 chemokine and MMP-2 metalloproteinase, and its pathological impact in a murine model of Chagas heart disease. Wild-type (WT) and OPN-deficient (spp1 −/−) mice were parasite-infected (Brazil strain) for 100days. Both groups developed chronic myocarditis with similar parasite burden and survival rates. However, spp1 −/− infection showed lower heart-to-body ratio (P
ISSN:	0925-4439 1879-260X
DOI:	10.1016/j.bbadis.2017.10.006